http://192.168.164.12:8010/api.php?action=feedcontributions&user=Qianpeng+Li&feedformat=atomLncRNAWiki - User contributions [en]2024-03-28T21:40:49ZUser contributionsMediaWiki 1.30.0https://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=GIHCG&diff=1276510GIHCG2019-08-15T02:15:43Z<p>Qianpeng Li: </p>
<hr />
<div><br />
==Annotated Information==<br />
===Name===<br />
Approved symbol: ''GIHCG''<br />
<br />
Approved name: GIHCG inhibitor of miR-200b/200a/429 expression<br />
<br />
Alias symbols: lncRNA-GIHCG<br />
<br />
HGNC ID: HGNC: 52649<br />
<br />
RefSeq ID:NR_038269<br />
<br />
Ensembl ID: ENSG00000257698<br />
<br />
LncBook transcript ID: HSALNT0289851<br />
<br />
===Characteristics===<br />
-<br />
<br />
===Function===<br />
[[File:GIHCG-exp1.png|right|thumb|400px|''GIHCG'' was highly expressed in TSCC samples.<ref name="ref2" />.]]<br />
[[File:GIHCG-exp2.png|right|thumb|400px|''GIHCG'' is upregulated in RCC tissues and indicates a poor prognosis.<ref name="ref3" />.]]<br />
* ''GIHCG'' promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429<ref name="ref1" />.<br />
<br />
* ''GIHCG'' increased tongue squamous cell carcinoma (TSCC) progression through negative modulation of miR‐429<ref name="ref2" />.<br />
<br />
* The deletion of ''GIHCG'' significantly represses cell proliferation and migration of renal cell carcinoma (RCC) cells<ref name="ref3" /><br />
<br />
===Regulation===<br />
-<br />
<br />
===Diseases===<br />
Hepatocellular cancer<ref name="ref1" /><br />
<br />
Tongue squamous cell carcinoma (TSCC)<ref name="ref2" /> <br />
<br />
Renal cell carcinoma (RCC)<ref name="ref3" /><br />
===Expression===<br />
The expression level of ''GIHCG'' was upregulated in TSCC tissues and cell lines<ref name="ref2" />.<br />
<br />
The expression level of ''GIHCG'' in the serum of renal cell carcinoma (RCC) patients is significantly upregulated compared with that in healthy controls. GIHCG is markedly increased in RCC tissues with advanced TNM stages. Furthermore, ''GIHCG'' expression is also significantly increased in RCC tissues with Fuhrman III and IV grades compared with that in Fuhrman I and II grades<ref name="ref3" />.<br />
<br />
{| class='wikitable' style="text-align:center"<br />
|-<br />
! | Experiment<br />
! | Forward primer<br />
! | Reverse primer<br />
|-<br />
| rowspan="1"|Quantitative real-time PCR<br />
| | 5'-CTTTCAAGAAGTTTGGCTGTC- 3'<br />
| | 5'-GCTCATTCAACGGATAAGTC- 3'<ref name="ref1" /><br />
|}<br />
<br />
===Evolution===<br />
-<br />
<br />
===Sequence===<br />
>NR_038269.1 Homo sapiens GIHCG inhibitor of miR-200b/200a/429 expression (GIHCG), long non-coding RNA<br />
<dnaseq>GGAGGAGTTACGCAGGCAGGGTTGTGGTTGCTGGCTGTTACCAGGACAACCGGAGGCGATTGACCGTTAT<br />
CTGCGGTTTGGAGCCGTTAGCGGGAGAGGCAGAGATATTCAGAGGTCTTTTAGGATGCGCTAAAGGGTCG<br />
TGAGGGCTCTCTTAAAATTTTCTTCACAAGCGGTTATCCAGTCGTGCCCCGCGGCCCTGCTGCTGGCCCC<br />
GGGGATCTGAGTCGTACCCTCTTGTTTTTCTCTGAGTCAGTCTTAAGGTGAAATGAAGTGTGGCCCAGTG<br />
GCTCCTCACTGTCGCTTCTCTAGTTTTCTGCCTCCTTTTAGAAAATTGAATTGAAAAGACAGGATGAAGT<br />
GGACACAGCATGTGAAGACAATTCTTTCAAGAAGTTTGGCTGTCAAGGAAAACAGAGAATGTGCTAAAGA<br />
ACATACAGACACAGAGCAGACAGGCCACCTTTGCAACCACATGGAGGTTTGTCTGATATTGAAGCTAAAG<br />
AAGCTAAGCTGGAAGACAGAGAGACCAAGTCCTGATGACATTGTTTGAACCCAGAGATCCAGACATGCCT<br />
GAAAACTAGTTTTACCACTGGACTTATCCGTTGAATGAGCCAATAAACTCTCTTTTATACTTAACCTTGG<br />
GTTTTACCTGGATTTTTGTCATTGACAGCTCAAAATATTCTAATATAGAAGTATACATCATTAAATCAAA<br />
AAAAAAAAAAA</dnaseq><br />
==Labs working on this lncRNA==<br />
*Department of Periodontology, Jinan Stomatological Hospital, Jinan, Shandong,China.<br />
*Department of Nephrology, The People's Hospital of Yichun City, Yichun, Jiangxi, China. <br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Sui C, Zhou Y, Shen W, et al. Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429[J]. Journal of molecular medicine, 2016, 94(11): 1281-1296.<br />
</ref><br />
<ref name="ref2"><br />
Ma L, Wang Q, Gong Z, et al. Long noncoding RNA GIHCG enhanced tongue squamous cell carcinoma progression through regulating miR‐429[J]. Journal of cellular biochemistry, 2018, 119(11): 9064-9071.<br />
</ref><br />
<ref name="ref3"><br />
He Z H, Qin X H, Zhang X L, et al. Long noncoding RNA GIHCG is a potential diagnostic and prognostic biomarker and therapeutic target for renal cell carcinoma[J]. Eur Rev Med Pharmacol Sci, 2018, 22(1): 46-54.<br />
</ref><br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=File:GIHCG-exp2.png&diff=1276509File:GIHCG-exp2.png2019-08-15T02:12:31Z<p>Qianpeng Li: GIHCG is upregulated in RCC tissues and indicates a poor prognosis</p>
<hr />
<div>GIHCG is upregulated in RCC tissues and indicates a poor prognosis</div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=File:GIHCG-exp1.png&diff=1276508File:GIHCG-exp1.png2019-08-15T02:07:00Z<p>Qianpeng Li: ''GIHCG'' was highly expressed in TSCC samples.</p>
<hr />
<div>''GIHCG'' was highly expressed in TSCC samples.</div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=CACNA1G-AS1&diff=1276507CACNA1G-AS12019-08-14T08:23:51Z<p>Qianpeng Li: </p>
<hr />
<div>==Annotated Information==<br />
<br />
===Name===<br />
Approved Symbol: CACNA1G-AS1<br />
<br />
Approved Name: CACNA1G antisense RNA 1<br />
<br />
Synonyms: CAS1<br />
<br />
RefSeq ID: NR_038439<br />
<br />
Ensembl ID: ENSG00000250107<br />
===Chromosome===<br />
17q21.33<br />
===Characteristics===<br />
-<br />
<br />
===Function===<br />
<br />
* It is reported that CAS1 appeared to promote calcium channel protein and type I collagen expression, and to have a positive effect on cell migration in human keloid fibroblasts<ref name="ref1" />.<br />
<br />
===Regulation===<br />
-<br />
<br />
===Diseases===<br />
-<br />
<br />
===Expression===<br />
CAS1 was significantly upregulated in keloid tissue<ref name="ref1" />.<br />
{| class='wikitable' style="text-align:center"<br />
|-<br />
! | Experiment<br />
! | Forward primer<br />
! | Reverse primer<br />
|-<br />
| rowspan="1"|Quantitative real-time PCR<br />
| | 5'-‑TGT GCT TCA CCA TGC TCC AT- 3'<br />
| | 5'-‑ATT AGT GCT CCG GCC AAC AA- 3'<ref name="ref1" /><br />
|}<br />
<br />
===Evolution===<br />
-<br />
===pubmed IDs===<br />
26397149, 29963160<br />
===Sequence===<br />
>gi|336176114|ref|NR_038439.1| Homo sapiens CACNA1G antisense RNA 1 (CACNA1G-AS1), long non-coding RNA<br />
<dnaseq>CAAACCCAGCTCGCTAACCGGCGCGGGCAGAGTACAGCTCCCAGGCTCCCGAAGCTTCCCACATCTGGAGGATGACGACCCTCCCCTGACCACATCTGGAGGGCGTCCAGCTGCGAGCCAGCGGGGCACAGCTCTCTTCTCCTGGCCTGGATCCCCACCCCCCCAACCCAGGAAGACTGAGAATCCCATCATCGCGTGCACATCTCATCCCAGGAGGGAGAGAGGAGCTGCCGAGTAGAAAGCAGACTGGCTGCAGGGACAGAAGACACCAAGGGCACCCTCCCCCACAGCTGCGCCTGGACCTCCTGCGAGAAGAGGAAGCCTTAGGGGTCTTTATTGTACCCTCAAGACCCCAGAGAGAAACAGAAGTGCTGAGGGGTCGCAGGCAGGTCTCTTACCCTCTCTGGGCCTCGAATATTTATCCATAGGAGGCTGAAGGTAACTGCCTTCGCAACTCATTCATGAGGGTCAATGGGACGACAGTGGCAAGAGGGGTTGGCACACTGCCCAGACTGTTCCAAAGCCAGGGCTGGGGCTGCCAAAAAGGCCACCTGTGCTTCACCATGCTCCATCCTCCCTCTCTTCCACCTCCCCAGGCTGGGCTCCACTTGTCCAGCTCTCTGACTTCCTGGCAAGGTTGAGTAGGCTCCAGCTAGGAAGGGGCCAGCTGACCTTGTTGGCCGGAGCACTAATCCCCTCCAGATGGGCTGGTGGCTTGCACTGAGGGCCTGGCTGCCCAGACAGAGCTGACTCTGGTCCCAGTGACCATGTGTGGCTATGTGTGACCGTGTGAAGGGAGCAATTCCATCCAGTCTCCCGGTTCCTTCCTGCTTCACTCCTCCCCACTGCTGACATCCCCCACAAGCAGTGGCCCCATGAAGGCCTTCTTGTCTCTAGTAGCCTCTTTTGGCTCTCTGTGTTGCTTAGCTGGAGGGCTGAGGATGCCTGGCACAGCCGATTCCCAAAGGCCTCAGAGGGACAGCTCCTCCCCCTGCTTCCCCCACCCCGTCAGCCCCATCACTCTGCACCTGCCCTTCCCAAAGCATGTGTCCCAGTCCCCATCCCTCAACCCAAGGAAGATGTATGTGTCAAGGACAGGACTCAGGAGCATTTCCCAACATTTAGGGGAAAGGATGAGGTCACAGGAAGGCTTTCTCTGCAGCAAGAAGGACTCAGATAGATTTGGGGAAGGACTTCCAACCCAACAGATGTTCCAAACGAAAGAGAACTCTTTCTTTGGACCAGCTTGTATGAAAGCAGACAAATGGACAACATGACCTCCTGCAAGGAGGCCCTGCTTCCATCCTTTCGAGGCTGGGGCTAGATGGATACCCCAAAAGAAATGTCTTAGTCGTGACAATAGCAGCTCCCACAATGCACCAGGGCATATGCAAAGTCACCATTCTGTGAAATATAAAAGCTCATATAAAGCAAAAAAAAAAAAAAAAAA</dnaseq><br />
==Labs working on this lncRNA==<br />
* Department of Integrative Oncology, Fudan University Shanghai Cancer Center<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Li Y, Liang X, Wang P, Long X, Wang X, Meng Z. Long non-coding RNA CACNA1G-AS1 promotes calcium channel protein expression and positively affects human keloid fibroblast migration. Oncol Lett. 2018 Jul;16(1):891-897.<br />
</ref>(1)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=FOXC2-AS1&diff=1276506FOXC2-AS12019-08-14T07:37:20Z<p>Qianpeng Li: </p>
<hr />
<div>==Annotated Information==<br />
===Name===<br />
Approved Symbol: FOXC2-AS1<br />
<br />
Approved Name: FOXC2 antisense RNA 1<br />
<br />
Synonyms: ODRUL<br />
<br />
RefSeq ID: NR_125795<br />
<br />
Ensembl ID: ENSG00000260944<br />
<br />
LncBook transcript ID: HSALNT0288979 <br />
===Chromosome===<br />
16q24.1<br />
<br />
===Characteristics===<br />
-<br />
<br />
===Function===<br />
[[File:FOXC2-AS1-exp.png|right|thumb|300px|FOXC2-AS1 was significantly upregulated in breast cancer (BC) tissues and cell lines.<ref name="ref1" />.]]<br />
<br />
[[File:FOXC2-AS1-fun.png|right|thumb|400px|Silenced FOXC2-AS1 caused cell cycle arrest and induced apoptosis<ref name="ref1" />.]]<br />
* Loss of function revealed that silenced FOXC2-AS1 significantly suppressed the proliferation ability, and flow cytometric analysis illustrated the influence of FOXC2-AS1 on cell cycle and apoptosis rate. Cyclin D1, cyclin D2, and cyclin D3 were all partly positively modulated by FOXC2-AS1 in breast cancer (BC).<ref name="ref1" />.<br />
<br />
===Regulation===<br />
-<br />
<br />
===Diseases===<br />
Breast cancer<ref name="ref1" /><br />
<br />
===Expression===<br />
FOXC2-AS1 was significantly increased in BC tissues and cell lines, and Kaplan–Meier survival analysis indicated that a high level of FOXC2-AS1 was associated with poor prognosis of BC patients<ref name="ref1" />.<br />
<br />
{| class='wikitable' style="text-align:center"<br />
|-<br />
! | Experiment<br />
! | Forward primer<br />
! | Reverse primer<br />
|-<br />
| rowspan="1"|Quantitative real-time PCR<br />
| | 5'-TTCATCGGCTGCGTATTCG- 3'<br />
| | 5'-TTGCCTTCTAGTCGCCTCC- 3'<ref name="ref1" /><br />
|}<br />
<br />
===Evolution===<br />
-<br />
===pubmed IDs===<br />
26408180, 29562954<br />
===Sequence===<br />
>gi|672890592|ref|NR_125795.1| Homo sapiens FOXC2 antisense RNA 1 (FOXC2-AS1), long non-coding RNA<br />
<dnaseq>CTTGCCGGGCTTCTTGTCGTCGCGGGGCACCTTGACGAAGCACTCGTTGAGCGAGAGGTTGTGGCGGATGCTGTTCTGCCAGCCCTGCTTGTTCTCCCGGTAGAAGGGGAAGCGGTCCATGATGAACTGGTAGATGCCGTTCAAGGTTTCCTTGCACCCTTCCTGGCTGTTCATCGGCTGCGTATTCGATTCTCAGCAAAAGGATGTTGAGACAACCCACCAGGCCTCTTCGCTTCGGCCTCTTCGCTTCGGGGAGGCGACTAGAAGGCAATGGGGCGTGCCACTTATTTCCAATAAAAGAACAGAAGACGAAAATGTA</dnaseq><br />
==Labs working on this lncRNA==<br />
* Department of Breast Surgery, the Affiliated Hospital of Guizhou Medical University, Guizhou, P.R. China<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Yang H, Chen T, Xu S, Zhang S, Zhang M. Long Noncoding RNA FOXC2-AS1 Predicts Poor Survival in Breast Cancer Patients and Promotes Cell Proliferation. Oncol Res. 2019 Feb 5;27(2):219-226.<br />
</ref>(1)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=File:FOXC2-AS1-exp.png&diff=1276505File:FOXC2-AS1-exp.png2019-08-14T07:29:28Z<p>Qianpeng Li: FOXC2-AS1 was significantly upregulated in breast cancer (BC) tissues and cell lines.</p>
<hr />
<div>FOXC2-AS1 was significantly upregulated in breast cancer (BC) tissues and cell lines.</div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=File:FOXC2-AS1-fun.png&diff=1276504File:FOXC2-AS1-fun.png2019-08-14T07:28:49Z<p>Qianpeng Li: Silenced FOXC2-AS1 caused cell cycle arrest and induced apoptosis</p>
<hr />
<div>Silenced FOXC2-AS1 caused cell cycle arrest and induced apoptosis</div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=EGFLAM-AS1&diff=1276503EGFLAM-AS12019-08-14T07:08:52Z<p>Qianpeng Li: /* Labs working on this lncRNA */</p>
<hr />
<div>==Annotation==<br />
===Name===<br />
Approved symbol: EGFLAM-AS1<br />
<br />
Alias: lncRNA-LOWEG, CTD-2108O9.1<br />
<br />
HGNC ID:HGNC:41169<br />
<br />
Ensembl ID: ENSG00000249491<br />
<br />
LncBook transcript ID: HSALNT0086786<br />
<br />
===Characteristics===<br />
-<br />
===Function===<br />
[[File:EGFLAM-AS1-fun.png|right|thumb|400px|Downregulation of long non-coding RNA (lncRNA)-CTD-2108O9.1 in breast cancer and its inhibitory effects on<br />
metastasis through its associated metastatic inhibitor leukemia inhibitory factor receptor (LIFR), epithelial-mesenchymal transition (EMT)-related genes and MMP family<ref name="ref2" />.]]<br />
*lncRNA-CTD-2108O9.1 represses metastasis by targeting leukemia inhibitory factor receptor(LIFR), which is designated as a metastasis suppressor in BC<ref name="ref2" />.<br />
<br />
===Regulation===<br />
-<br />
===Diseases===<br />
Gastric cancer<ref name="ref1" /><br />
<br />
Breast cancer<ref name="ref2" /><br />
<br />
===Expression===<br />
Significantly reduced expression of lncRNA-LOWEG was found in gastric cancer tissues and cell lines (SGC-7901, AGS, BGC-823 and HG-27) compared with patient-matched nontumorous adjacent tissues (P < 0.01) or the normal gastric cell line GES-1 (P < 0.05). Lastly, western blot and real-time PCR analysis suggested that lncRNA-LOWEG is positively correlated with the expression of leukemia inhibitory factor receptor (LIFR) gene at the translational level<ref name="ref1" />.<br />
<br />
RNA-CTD-2108O9.1 is downregulated in Breast cancer (BC) tissues and cells and acts as a metastatic inhibitor of BC<ref name="ref2" />.<br />
===Evolution===<br />
-<br />
<br />
==Labs working on this lncRNA==<br />
*Department of Surgical Oncology and General Surgery, The First Hospital of China Medical University, Shenyang, 110001, People's Republic of China.<br />
<br />
*Department of Breast Surgery, The First Affiliated Hospital of China Medical University, Shenyang, China<br />
<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Zhao J, Sun J, Song Y, et al. A novel long noncoding RNA-LOWEG is low expressed in gastric cancer and acts as a tumor suppressor by inhibiting cell invasion[J]. Journal of cancer research and clinical oncology, 2016, 142(3): 601-609.<br />
</ref>(1)<br />
<ref name="ref2"><br />
Wang M, Wang M, Wang Z, et al. Long non‐coding RNA‐CTD‐2108O9. 1 represses breast cancer metastasis by influencing leukemia inhibitory factor receptor[J]. Cancer science, 2018, 109(6): 1764-1774.<br />
</ref>(2)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=EGFLAM-AS1&diff=1276502EGFLAM-AS12019-08-14T07:08:28Z<p>Qianpeng Li: </p>
<hr />
<div>==Annotation==<br />
===Name===<br />
Approved symbol: EGFLAM-AS1<br />
<br />
Alias: lncRNA-LOWEG, CTD-2108O9.1<br />
<br />
HGNC ID:HGNC:41169<br />
<br />
Ensembl ID: ENSG00000249491<br />
<br />
LncBook transcript ID: HSALNT0086786<br />
<br />
===Characteristics===<br />
-<br />
===Function===<br />
[[File:EGFLAM-AS1-fun.png|right|thumb|400px|Downregulation of long non-coding RNA (lncRNA)-CTD-2108O9.1 in breast cancer and its inhibitory effects on<br />
metastasis through its associated metastatic inhibitor leukemia inhibitory factor receptor (LIFR), epithelial-mesenchymal transition (EMT)-related genes and MMP family<ref name="ref2" />.]]<br />
*lncRNA-CTD-2108O9.1 represses metastasis by targeting leukemia inhibitory factor receptor(LIFR), which is designated as a metastasis suppressor in BC<ref name="ref2" />.<br />
<br />
===Regulation===<br />
-<br />
===Diseases===<br />
Gastric cancer<ref name="ref1" /><br />
<br />
Breast cancer<ref name="ref2" /><br />
<br />
===Expression===<br />
Significantly reduced expression of lncRNA-LOWEG was found in gastric cancer tissues and cell lines (SGC-7901, AGS, BGC-823 and HG-27) compared with patient-matched nontumorous adjacent tissues (P < 0.01) or the normal gastric cell line GES-1 (P < 0.05). Lastly, western blot and real-time PCR analysis suggested that lncRNA-LOWEG is positively correlated with the expression of leukemia inhibitory factor receptor (LIFR) gene at the translational level<ref name="ref1" />.<br />
<br />
RNA-CTD-2108O9.1 is downregulated in Breast cancer (BC) tissues and cells and acts as a metastatic inhibitor of BC<ref name="ref2" />.<br />
===Evolution===<br />
-<br />
<br />
==Labs working on this lncRNA==<br />
*Department of Surgical Oncology and General Surgery, The First Hospital of China Medical University, Shenyang, 110001, People's Republic of China.<br />
<br />
*Department of Breast Surgery, The First Affiliated Hospital of China Medical<br />
University, Shenyang, China<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Zhao J, Sun J, Song Y, et al. A novel long noncoding RNA-LOWEG is low expressed in gastric cancer and acts as a tumor suppressor by inhibiting cell invasion[J]. Journal of cancer research and clinical oncology, 2016, 142(3): 601-609.<br />
</ref>(1)<br />
<ref name="ref2"><br />
Wang M, Wang M, Wang Z, et al. Long non‐coding RNA‐CTD‐2108O9. 1 represses breast cancer metastasis by influencing leukemia inhibitory factor receptor[J]. Cancer science, 2018, 109(6): 1764-1774.<br />
</ref>(2)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=File:EGFLAM-AS1-fun.png&diff=1276501File:EGFLAM-AS1-fun.png2019-08-14T07:06:18Z<p>Qianpeng Li: Downregulation of long non-coding RNA (lncRNA)-
CTD-2108O9.1 in breast cancer and its inhibitory effects on
metastasis through its associated metastatic inhibitor leukemia inhibitory factor receptor (LIFR), epithelial-mesenchymal transition (EMT)-relat...</p>
<hr />
<div>Downregulation of long non-coding RNA (lncRNA)-<br />
CTD-2108O9.1 in breast cancer and its inhibitory effects on<br />
metastasis through its associated metastatic inhibitor leukemia inhibitory factor receptor (LIFR), epithelial-mesenchymal transition (EMT)-related genes and MMP family</div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=ZNF667-AS1&diff=1276500ZNF667-AS12019-08-14T03:11:04Z<p>Qianpeng Li: </p>
<hr />
<div>==Annotated Information==<br />
<br />
===Name===<br />
Approved Symbol: ZNF667-AS1<br />
<br />
Approved Name: ZNF667 antisense RNA 1 (head to head)<br />
<br />
Synonyms: MORT<br />
<br />
Ensembl ID: ENSG00000166770<br />
<br />
RefSeq ID: NR_036521<br />
<br />
LncBook transcript ID: HSALNT0289293<br />
===Chromosome===<br />
19q13.43<br />
===Characteristics===<br />
-<br />
===Function===<br />
<br />
* MORT might play a tumor suppressor role in cancers <ref name="ref2" />.<br />
<br />
===Regulation===<br />
-<br />
===Disease===<br />
Cancers <ref name="ref1" /> <ref name="ref2" />.<br />
<br />
===Expression===<br />
ZNF667-AS1 is expressed in all normal cell types, but epigenetically silenced during cancer-associated immortalization of human mammary epithelial cells<ref name="ref2" />.<br />
<br />
===pubmed IDs===<br />
26646903, 29707199<br />
===Sequence===<br />
>gi|302488598|ref|NR_036521.1| Homo sapiens ZNF667 antisense RNA 1 (head to head) (ZNF667-AS1), transcript variant 1, long non-coding RNA<br />
<dnaseq>AGAATCCACCGGGGTGCAGCGAGGCTGTGGAAAGTCCCACCCAGAACGTGAGGTGAAGAAGGCTTGGGCTGCGCTGGTTCTGCTCTGTCCGGGTCGGAGATGAACTGACCCGGGAGAGCAGCGGAGGGATGTTTCTTTTGGCCAACAGTGGGGACTCACCTGCACGTTTTGCGAAGAGGCCCACAGTCCTTTGCGTGGCGCTCGGACTACATTTCCCAACGGCCCCTGCACGCCCTGGGGGCTGTTCCATGCGGTGTTGCGCCTGCGTAGCCGGCGGGCTGGCAGTGAGACTGACTGCGTCGGGGTTGAGACTGGGTGGATGAGGCTCACCCCGGCGGGGAGAAGGGACGAGGAGGGGCGGACAGCGGAAGGTCCGGGAGTGTCCGCCATAAAGTCGTTTGAGGTGACCGTTGCGTAATTGTGAGTCTGTGAGAGAAGATGTGAAGTATGGCCTCGTCCCGGTCATCTGGGCGTGCGGGTCCCGGGTTTTGATCGCGCGTTTGTGTAGTTTTAACTTCTAGTCATGGCGAATGATCGCAGGAGAGCACAGACTGGACCCTGCTACGATCTCTCTTGGAGTGGATCAGACTGATGATCACCAACAACCAACTCATTCCCGGATAAGGAAGAAGAGAGTGTCACCTACTTCAGTGTGGTTTCAACCCTACTTCTGCATCTTAAAGACACTGTATGGTTTCAGCAGTAGTGCCCCTGTTCATTAGTCCCCCTGATGTTTTCATTCCTCATCTCATCTTTTTCTTAGCAGCATTCAATGAATCCTTCATTCTAGAAACACTCTATATCTTTGGTTTTCATGAGACCATTCTCACCTTGTTTTGTCCTGTGACTTTTTTGAAAAAAACAAAAACAAAAAACCCTTTTTTTCTTTTTAAATTCTGGTAAAAAACACAATGAAAATTTGCTATCTTAACCATGTTGAAATGTGCAGTTAGTAAAGTACATTCACATTGTGGTGCAAGCCATCACTACCATCCATCACTAGAACCCTTTTCATCTTGCAGATCTGAAACTCTACCCATTAAACGACTTCCCATCTTCCCATCCCCACAGCTCCTAGCAACCAACATTCTACTTTCTCTATCAGTTTGACTACTCTAGGTACCTCATATGAGTAGAATCATACAGCATTTATCCTTCTCTGCCTGGCTTATTTCACTTGTATAATGTCCTCAAGGTTCATTCATGTTGTAGCATGCATCAGAACTTCCTCCCCTTTTAAAGGCTGGATAATATTTCATGGTATGTTTAGATCACATTCTGTTTATCCATTCATCCATCAGTGAACACTTGTGCTCCTTCCAACTTTGGGCTGTTGGGTGTCCTGCCACTGTTGCTCCTAGTGCTCAATCTCGTTTATTCCCTCCTAATCAAGTGTACAACGTTGGACACTGTGCAGGATGATGCCACTTCATCTTGGATGCTAATCTGCCATGTTGACTTCTGATTAACCCCAGGCCCAGGAATGCCTCAAGATTTCTACTTTACTTACTGTTGCTTGTGTAAGCCAAGACAACCTTGATGTTATCATAAACATGTACTTACCTAAGTCCTGTCCTTTGGCAAATTATGGGCTATGAGACACAGCATTCTTGCCTTTCCCTGAGGGGTCAATTTCAGCGATCCTACACATTCCTTCTGAAGCACTTATGCTCTTTCTATATGGTATGTAAGCTCTCGGTCTGGGGAGTAACAGTGCAGAGATCTACCTGTCTTGTTGCCACATGTTTCTAAACTTTCCAATAAATCACCTTCTACTGACAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAA</dnaseq><br />
==Labs working on this lncRNA==<br />
* The University of Arizona Cancer Center, Tucson, AZ, 85724, USA<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Vrba L, Garbe JC, Stampfer MR, Futscher BW. A lincRNA connected to cell mortality and epigenetically-silenced in most common human cancers. Epigenetics. 2015;10(11):1074-83. <br />
</ref>(1)<br />
<ref name="ref2"><br />
Vrba L, Futscher BW. Epigenetic silencing of lncRNA MORT in 16 TCGA cancer types. F1000Res. 2018 Feb 21;7:211.<br />
</ref>(2)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=LIFR-AS1&diff=1276499LIFR-AS12019-08-14T02:51:30Z<p>Qianpeng Li: </p>
<hr />
<div>==Annotated Information==<br />
<br />
===Name===<br />
Approved Symbol: ''LIFR-AS1'':LIFR antisense RNA 1<br />
<br />
RefSeq ID: NR_103553<br />
<br />
Ensembl ID: ENSG00000244968<br />
<br />
RefSeq ID: NR_103553<br />
<br />
LncBook transcript ID: HSALNT0288975<br />
===Chromosome===<br />
5p13.1<br />
<br />
===Characteristics===<br />
-<br />
===Function===<br />
* ''LIFR-AS1'' knockdown attenuated, whereas miR-29a inhibition enhanced the cellular effect of PDT on HCT116 cell proliferation and apoptosis. Furthermore, TNFAIP3 was confirmed to be a direct target of miR-29a and exerted a similar effect to ''LIFR-AS1'' on the cellular effects of PDT. In a word, ''LIFR-AS1'' serves as a competitive endogenous RNA (ceRNA) for miR-29a to inhibit its expression and up-regulate downstream target TNFAIP3 expression, finally modulating the resistance of CRC to PDT<ref name="ref2" />.<br />
<br />
===Regulation===<br />
''LIFR-AS1''and miR-29a negatively regulated each other<ref name="ref2" />.<br />
===Diseases===<br />
''LIFR-AS1'' is associated with higher rates of preterm birth <34 weeks<ref name="ref1" />. <br />
Colorectal Cancer (CRC)<ref name="ref2" /> <br />
===Expression===<br />
lncRNA ''LIFR-AS1'' was upregulated in PDT-treated HCT116 cells<ref name="ref2" />.<br />
<br />
===Sequence===<br />
>gi|511773009|ref|NR_103553.1| Homo sapiens LIFR antisense RNA 1 (LIFR-AS1), transcript variant 1, long non-coding RNA<br />
<dnaseq>GCGCGCGGGTGCTCCAAGGAGTCGGAGGAACGCGGCCGCGCGACGGGCCCCGGACGCCGAGGGTGGTGCTTCCTCCGAGCCTCCGGTGGTGAGGCCGCTCTCAGAAGGTCATGGAAGCGCAGGGGAGAGCGAGGCGGCCGAGCCCAGGCAAATCCTCGAGAAAGGCCGAGTGCGCGACGGCTCTGCGGGGAGGACCGCGCCTCCCCGAATGCGGCCGCTGCTGCCGCTGCAAACAGTGCCTTGAGGAGAGGAAAGCGGGGAACCGTGTTTTCGCCGCCTCTGTAACCACTGCACACAAGAAAACCAGCTTCTGGGAGAGGGGGATGATTGTTGGGACTTTGCGAATTACCTAAACAGCCCAGGGCCGAGGCGCCGCCGCTCGCGTCCTGGTCCTCCTGCCGGGTGTGGGGCTCCCCTGCCCGAGATGGCCAGCGGGCGCGCCGAGAGTATCCTGGAGCCATCTAGTCTTGCCTCGGAGGCGGGGTGGGCTTATTTGTGCGGAGAAGAAACGGATCTCTTAATGGGGTGAGATTTTTCCTCCGTACATTGTTCCCATTTCCGCAGTTTCACTTGGCCTCGGTTTTCTAGCAGAGTAATCACCAAATGAAATTAGCTGGAGAGCGTTTGATGGCGCAGAATCACGGTCTGAAGATGTTTACGCTGTATGCCGGACGCGTTTGATGGTGTTCTCTTCGGCACAATTAATTTTGCAAAGTTCAGAAATGTGCCAGACAGAGCCCCTGGCACGCAGTCAGGACTCTACAGACACACCTTGAGTAGGAAACAGGCTTGTTTGTTTCATCTGTGATTTATGTGATGCACCAGCACCAAGGCCAACGTGTTTTTTAAAGACCTTTCGATGAAACTCCAAAGCAATTTATAAATTGGCAAAATGAAGCTTGTTTTGTAAAATAACTCTTCCTTGTTGATCATGTAATTAAATGGGCAACAAAACACCTGAAAGGACATTTACTGAAAAGTAGACTCCCAAAACAAAAATATGTATTTCACAGCTAGATACGGTCGCTATTAGCGTCCTAATGGCCAACTCCATCCATGTGCGTATTTTGAACACTAAAAACGCCTCCTGTTACCCCTAAGACCTTGTTTGGATAACATTTTTCTATTATAAGTACTCGAAACCAACCCCATTTAAGATGTTTACCCTTATTCTTGAGTCCTTGATGGTTTGGGAAATTTATCATTATTCATATTGCACAATCCTGTCACTGTCTTTTCCATTAGGCACAGTGCCTAAGGTCCACAATATTTTTAGAGGCCCACAAAAAATATTTTAATTTCTTTTCAAATCAGAAGGAAAAAAAATTTAGGTTTAAGAAAGTATTTTAATATATATTAATATATTTGTTTTTGTGCTAATACAATCTTAAAATGTATGTATATATGTGTGTGTGTATATGTATATATATTTTAATGGAGTAAGGGGCTCAACGAAGGCAAAAAGGCCTAGAGCCCAAGAAAAACATGATGTGGCCCTGTTGCCTGGGGTTGAAAAATCCCATTCCATGAGAAGAATTTAGTTTTAAGAATATTACATAAAATGCTCATTTCTGTGGCCTTGCTATAATAGAAAGATGGAGATTCAGAGTAGTGATAATGGCTAACATCCACCTGATACACACCATGTGTCCATTACCTCTTAATCCTCACAGCACACCTGTGAAATAGGTACTATTCTCACACTTAGGGGGTAATGCAGGTTTTGTGGGGCCTGCAATTTATGCAATTTGGGTGGTCCTCTTAAAGAAAAAGCAAATACTGTGTATTAGTCCGTTCTCACACTGCTATAAAGAACTGCGCGAGACTGGGTAATTTATAAAGGAAAGAGGTTTAATTGACTCACAGTTCCACATGGCTGGGGAGACCTCAGGAAACTTAACAATCGTGGTGGAAGGAGAAGCAAGTACCTTCTTCACAAGGAAGCGGAAAGAATTGTGAGCGGAGGAACTTGCCAAACACAAAACCGTCAGATCGCGTGAGAATTCAGTTACTATCACGAGAACAACACGGGAAAACTGTCCCCATAATCAAGTCATTTCTCTCCCTAACAAGTGAGGATTACAATTCAAGATGAGGTTTGGGTAGGAACACAAAGCCTGACCCTATCCCACAGCATGTCCAGGCTGCCCTAGCACCACCCAATAGAAGGGAAAATGGCAGAGGGAAAGTCCTAGTGGAAAGAGACCTCAGTCTCAGCTAATTGTGGTGACAATATATTGCTTTTGCAAATTGTACATAAACATATGACCAGGTGAATGTATCGCCAAGGCTCCTGCCAAGGCCTGGGATGGAGGCCTAGAGAAGATGCCCGAAAGTTTATGCTGTGTGAGCTTCACAGAAGACCTGCCTTCCATGTATACCCATTTTACAGGTGTCTGTGCGGTGCAGAAACTGTACAACTGTATACAGTGACCATTTCTACTCTGGGTCTCTAAACAAGGGCTGGTATCGTTACAGAGACTGAAGACTGAGGAAGACCATCTCTGTAGGATGCCAAGGATTGACTGGAGAAAGTCTGGCAGAATAGAACGTCTTGCACAAGAGGAGTGGAACAGCGGTCAGAGCATTACAGCTGACTCATCTTGACCAGAGAAGGTTACAGCTGGAGGCCCCAGAGATTGCCCACTTCCCCCCTCCATTTGACAGCAAGGGAAACAATGGCCAGAGAGGATCTGGAACTTTCTCTCAATTTCAGTGAAGGCCAGAGGTAAAATCAGGATTGTCTGAAGACAAGTAAGGTCAGGTGCATAGGGTTATATGTAGGAGTATAGTTAACAGGTGTCAGAAACTTGGATTTAATTTAGAGGTGGTTAGGACATGCATAATATTTTTCAACTATGCGTGAAATCTGGGATTCTGCATTTATTTAAAATATAGGATTGTCCATTAATTCTTTCTCTTGAGAGGGCGCTTCTTTCAGAAATGATCTAGGCACTTACAAACATTTTAAAAATATATACACGTGAGATCATACTTTCATAGTGATATAAGCATCATTGCTCATATCCCTAATGAACAGATGGGGAAAAGGAGGTAGAGACAGAGAGAGAGACAGAGAGTCAGCAACTCACCACAAGAATCTCCTGGTTGCCTGTCTGGGCTTCTGTCAGCTCCATTTAGTTGAATTTCTATTCAATATTATTACTGAGGTCTTATACTTAAGAACATGTTCTTTGGGTTTCCTGCTTATCTCCAAGCTGAAGAATTTATTTTCTTCTATTTGCTTTTCCAATCTTCAGCTTCCATGACCTTAAAAAAAAAAGTACACAAACTGAGCTGGTCTAAGAGCAGCCTGTTTGCAACCTGATATGAGACCTGGAATGCAACCAGATAAACCTTGGTGTAGGGTTCTCTAAACACATTCAACATTTTTTCCAAGAGGCAATCGGTTTATTTCCTTTGAAATGCTTGATGATGAATTAACAGTACATTTTCGAAACTATTGAAAGAGCAGAGGTAAAATGGTAGTTATACATGTCGGAATGGGAAATAGAGAACTATGGAATTTATCTTACTTTGAAGCTTAAACCCCTTTTAATATTCCTTGTATTTAGCCACATGTATTTTTAAGGTGGAAATTAGTTAATGGAATATTCTCATAGTCCATACTTTTTATTAAGGTTGATGTTTGATGAACCAGATAATGTCTACTCACTTTCTGCTTTAAAGTTTATAATTCTTGATAAAAGGAAAAGTGGTGAATTATGTGAGCCAACCCTGGAAAGTATTTCCGTATTGAGTTTTGTTTGTTTCAAAGAACCTACTGTACATATGCAAAAAAA</dnaseq><br />
<br />
==Labs working on this lncRNA==<br />
* Department of Obstetrics and Gynecology, Ohio State University, Columbus, OH. Electronic address: Heather.Frey@osumc.edu.<br />
==References==<br />
<references><br />
<ref name="ref1">Frey HA, Stout MJ, Pearson LN, Tuuli MG, Cahill AG, Strauss JF, 3rd, et al. Genetic variation associated with preterm birth in African-American women[J]. American journal of obstetrics and gynecology. 2016.<br />
</ref>(1)<br />
<ref name="ref2"><br />
Liu K, Yao H, Wen Y, Zhao H, Zhou N, Lei S, Xiong L. Functional role of a long non-coding RNA LIFR-AS1/miR-29a/TNFAIP3 axis in colorectal cancer resistance to pohotodynamic therapy. Biochim Biophys Acta Mol Basis Dis. 2018 Sep;1864(9 Pt B):2871-2880.<br />
</ref>(2)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=FEZF1-AS1&diff=1276498FEZF1-AS12019-08-14T01:31:50Z<p>Qianpeng Li: </p>
<hr />
<div>==Annotated Information==<br />
===Name===<br />
Approved symbol: FEZF1-AS1:FEZF1 antisense RNA 1<ref name="ref1" /><br />
<br />
HGNC ID: HGNC:41001<br />
<br />
Ensembl ID: ENSG00000230316<br />
<br />
RefSeq ID: NR_036484<br />
<br />
LncBook transcript ID: HSALNT0288975<br />
<br />
===Characteristics===<br />
FEZF1-AS1 is a ~2.6-kb RNA transcribed from the plus strand of chromosome 7 <ref name="ref1" /><ref name="ref2" />. FEZF1-AS1 is transcribed from the opposite strand of FEZF1 protein (7q31.32), and there are 611 nucleotides of full complementarity between the frst FEZF1-AS1 exon and FEZF1 exons 1 <ref name="ref1" />.<br />
<br />
===Function===<br />
[[File:FEZF1-AS1-1.JPG|right|thumb|400px|'''''FEZF1-AS1''''' regulates GC cell proliferation<ref name="ref2" />.]]<br />
<br />
*Dysregulation of FEZF1-AS1 participates in colorectal tumorigenesis and progression, which might be achieved, at least in part, through FEZF1 induction <ref name="ref1" />.<br />
<br />
*FEZF1-AS1 could act as an "oncogene" for gastric cancer partly through suppressing P21 expression; FEZF1-AS1 may be served as a candidate prognostic biomarker and target for new therapies of gastric cancer patients <ref name="ref2" />. FEZF1-AS1 is overexpressed in gastric cancer, and upregulated FEZF1-AS1 expression is correlated with larger tumor size and higher clinical stage; additional higher expression of FEZF1-AS1 predicted poor prognosis <ref name="ref2" />. FEZF1-AS1 could epigenetically repress the expression of P21 via binding with LSD1 (a demethylase) <ref name="ref2" />.<br />
<br />
[[File:FEZF1-AS1-fun.png|right|thumb|400px|An illustrative figure detailing the relationship among FEZF1-AS1, miR-610 and Akt3.<ref name="ref3" />.]]<br />
*FEZF1-AS1 inhibition reduced myeloma (MM) cells proliferation, arrested cell cycle in G0/G1 phase and induced cell apoptosis. Furthermore, FEZF1-AS1 promoted MM cells progression by regulating miR-610/Akt3 axis<ref name="ref3" />.<br />
<br />
===Expression===<br />
FEZF1-AS1 is overexpressed in gastric cancer, and upregulated FEZF1-AS1 expression is correlated with larger tumor size and higher clinical stage; additional higher expression of FEZF1-AS1 predicted poor prognosis <ref name="ref2" />.<br />
<br />
Expression of FEZF1-AS1 was upregulated in myeloma (MM) samples and cell lines<ref name="ref3" />.<br />
<br />
===Disease=== <br />
*Colorectal carcinoma<ref name="ref1" /><br />
*Gastric cancer<ref name="ref2" /><br />
*Myeloma (MM)<br />
<br />
===Sequence===<br />
>NR_036484.1 Homo sapiens FEZF1 antisense RNA 1 (FEZF1-AS1), long non-coding RNA<br />
<dnaseq>GAAAACTTTGGGCTTGGCATTAGGAGAGCCTCGGCTGAAATCCGAGGTTTTGAACGCGATTTTTTCCGAC<br />
AGAAGCTGGGCGCTTTCTTTCATGTAATGCTGCAGCTGAGCCTGGGACAGGTCTTTGAAAGCTACTCCAG<br />
AAGGGTATTTCTCCACCGCCGGGACCACCAGTTTATTCCTTTCGGCTAAATACGTTTTTGGCTGCGGGTG<br />
CAAAGGGGAACTGAGGAAGTAGGAGGCCACCGGGTGGATGTTCACGCCGGCTGCCGGGTGGCATGGGCCG<br />
TCACCTCGGTTCAGGTAGCACAAGGCGCCCATGGCGTGGAATGAAGAGTGGTTGACCACACGCGGCCTTA<br />
CCAGCTTGTACTGCTGCAGCGGCAGCGCGTCGCGGGCCAGGTCGCCCTTGAGACTCAGTGCGCAGTTGAG<br />
CAGGTCGCTGCAGCTGAATGCGGGAGCCGAGGGCACCGCCGCGGGCGCCGCCGGGGCCTCCAGACTGGCC<br />
TTCCGCGGCTCGGAGCCCGTCACTCCTGCCTTGGGGCTCGTGTCGTAGGCCACAGGCACGAAGGGGATCA<br />
TGCAGGGGATCGACGAGTTGAGATGCAGAGAGTGCTTGGGTTCCCCCTTGGCATCACCAGCCGAACCTGC<br />
CTGCCCAGCCCAATGGACTCCTGCCAGCCCATCGCAGAGTTCTTGGCGCACCAATGACTCGGGGACAATC<br />
ACTACTTATTTCTATCAATAGAAAGTGTTGTGTCAATAACGCAGCCAAGATCTCGCCAATCGTTAACTTC<br />
CAAGAGGAGAAGGGCTCGGGGTTGCCCGCTCCCGGAATCCCGGAGTCTCCGCGGCCCGAACCGAGTCTGG<br />
ACCATTTAGAAGACGCCGGCAGGTAACTGGCCTCCCCAAACGCCCCGAAAATTAAAAGCCTTAGGAGGCT<br />
TGTTCTGTGTTTGTGGTTTTGTAAAGGCAATGCCCGCGGCAATAGGCCTGGGAAAGTCGCACTTTCATCC<br />
ACAAAGTTGAGGAGTTGCAAGGAATAATTGGGTGTCACACCACAAGCAACCTTGACTCGATCGGACCCCA<br />
CCCAGGATACACACAGACGCGCGCGCGCGCACGCTTCCGAGTTTCCATTGAGAGTCTGGAAAGAGCATTT<br />
CTTTCTTAAGTACCTGCGCTCAGCTAGAGCTCTCCCGGAGCATTTTAAATACTGAATGCCGAGCGGAGAA<br />
GGGAAACAGAGTGTATTAATCCCCACTCCGGTTGCCGGTGTCTGCAAGCCTCCTCTAAGCAGCGCAGGCG<br />
GCAGCCTGGATGTCTGTGCGCATCAAGGAGACTTGCCGGCGCCAGAGTTGTGTCCACAGGTGCACTTGTG<br />
CCTCCCAAAGAGCGCGCGTAGAGACCATTTCCCCTGCAACGCCCCCCAGCCGAACACCCGCCGGGTGTGG<br />
CACCTCGGCCGAAACTCCTGGGGCGGCGCGGTGGAGCGTGTGGAGGTTTCCGGGAAGACGCCTACGGCTG<br />
CGGCTCCGACTGTGCGGGCTCCCGCCGCCCAGGCAAGAGCGTCCAGGAGCGCGCTGGAAGCTGCGGCGCG<br />
CACCTTCCCCGGCGCAGTCTCTTGCCAGCCGGCGATCACGCAGAGCTGAACCCCGCAGCTAGGCGCGCAG<br />
GAAGGGCTGCACAGAGTTTGAAGACACGGCAGCTGTAAGCTGGCGTGAGGAGGCCAAAGGAGCGCGCAGA<br />
GCTGCAAGCAAAGGGCGGTGGGGCCTGGACCCTGAAGTGAGTGGCCGACCGCAGCAGCTCAAGGTGCCAT<br />
CTGCCTGGCAAGCTACCCGGGTCCCTCCGCCCCACTCTAACTTTCCGCGAAAATCAGTTCCGCCTCTGCC<br />
CCAAGAGCCAAGAGGGGTGGAAAGGAAGAGAGCTTGGGCTGGGAACGCGCCTGATGTCTAACAGAAAGGC<br />
AGTGGCAGCTGGCGAAAAATCCCCCTCCTGCTGCACTCCTCCGCCACCGGGCTAGGTTGAAAGGAAAAAG<br />
CCAAGAAGCGCGAAGCAGCCCGGCTCTGGAAGGCTTTGGAGAGTCCAGCTGACTTGTACACAATTCGCGG<br />
CCTCTGGAGCCTTACCTGCCTTCTTGACTGAATGCCACCAGTTCGTTTTACGCTTGTGGCTTTTTGTTGA<br />
AGTCCCTATCATAAGCAAATGCAGTTTCTGGCTATGGTTACTGCAATTCGAAATAAAAGGCCTGTGAGGT<br />
GTGTCCCTCCAGACTGAGAGGCTATGACTCAGGGTTGGACTTTATGGAAAAAAAGAAGTTTATAAAACAA<br />
GTAACCCAGTTTCTCCAACCTTTACTGTGGAGCAACAGCGTCAAGCAACAAAACCCAGCAAAGTTTTGCT<br />
TGTCACTTACAAGGGTGTTACTGAAATCTGGAAGGCGAACAATTAGAAGATAGCCCAAACATGCTCTATT<br />
GCTCTACACTGAAATACTTGCCTCCAATAATAGAAAAAACCTGTTTTCGTGCAATTGATTGATTAGCGTT<br />
CTGCAGCAGTCCCTGGACAATTTTAAAGACATTTTGTGTTTGTGGCCAAAATTAGAAACAAGCAGACACA<br />
CACACAAAACAACCATATTCAAGACACGGTTCGACTGTTTCCTTGACACTACCCACGAAGTTTAAAGCAT<br />
TTTTTATGTTATTTTCAAACTTTCTTAAGTGATCCCATGAAATAAAAGTCGATAATAGAAATT</dnaseq><br />
<br />
==Labs working on this lncRNA==<br />
*Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.<br />
*Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China<br />
*Department of Pharmacy, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.<ref name="ref1" /><br />
*Department of Oncology, Zhongda Hospital, Medical School, Southeast University, Nanjing, Jiangsu, People's Republic of China.<br />
*Department of Laboratory, Affiliated Chest Hospital of southeast University, Nanjing, Jiangsu, People's Republic of China.<br />
*Department of surgery, Affiliated the second hospital of Bengbu Medical College, Lianyungang, jiangsu, People's Republic of China.<br />
*Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, Jiangsu, People's Republic of China.<br />
*Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, Jiangsu, People's Republic of China. lyw0171@outlook.com.<br />
*Department of Oncology, Zhongda Hospital, Medical School, Southeast University, Nanjing, Jiangsu, People's Republic of China. wangcailian65@hotmail.com.<br />
*Department of Gastroenterology Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, People's Republic of China. nyefygz@163.com.<ref name="ref2" /><br />
<br />
<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Chen N, Guo D, Xu Q, Yang M, Wang D, Peng M, Ding Y, Wang S, Zhou J. Long<br />
non-coding RNA FEZF1-AS1 facilitates cell proliferation and migration in<br />
colorectal carcinoma. Oncotarget. 2016 Mar 8;7(10):11271-83.<br />
</ref><br />
<ref name="ref2"><br />
Liu YW, Xia R, Lu K, Xie M, Yang F, Sun M, De W, Wang C, Ji G.<br />
LincRNAFEZF1-AS1 represses p21 expression to promote gastric cancer proliferation through LSD1-Mediated H3K4me2 demethylation. Mol Cancer. 2017 Feb 16;16(1):39.<br />
</ref><br />
<ref name="ref3"><br />
Li QY, Chen L, Hu N, Zhao H. Long non-coding RNA FEZF1-AS1 promotes cell growth in multiple myeloma via miR-610/Akt3 axis. Biomed Pharmacother. 2018 Jul;103:1727-1732.<br />
</ref><br />
</references><br />
<br />
<br />
<br />
<br />
[[Category: Antisense]]</div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=File:FEZF1-AS1-fun.png&diff=1276497File:FEZF1-AS1-fun.png2019-08-14T01:29:24Z<p>Qianpeng Li: An illustrative figure detailing the relationship among FEZF1-AS1, miR-610 and Akt3.</p>
<hr />
<div>An illustrative figure detailing the relationship among FEZF1-AS1, miR-610 and Akt3.</div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=LAMC1-AS1&diff=1276496LAMC1-AS12019-08-13T08:35:21Z<p>Qianpeng Li: </p>
<hr />
<div><br />
==Annotation==<br />
===Name===<br />
Approved symbol: LAMC1-AS1<br />
<br />
Approved name: LAMC1 antisense RNA 1<br />
<br />
Alias symbols: lnc-LAMC2-1:1<br />
<br />
HGNC ID: HGNC:52645<br />
<br />
Ensembl ID: ENSG00000224468<br />
<br />
LncBook transcript ID: HSALNT0018525<br />
<br />
===Characteristics===<br />
-<br />
===Function===<br />
<br />
*Rs2147578 in lnc-LAMC2-1:1 might be a genetic modifier for the development of colorectal cancer(CRC)<ref name="ref1" />.<br />
*The lnc-LAMC2-1:1 rs2147578 polymorphism may be a risk factor for developing childhood acute lymphoblastic leukemia (ALL)<ref name="ref2" />.<br />
<br />
===Regulation===<br />
-<br />
===Diseases===<br />
Colorectal cancer (CRC)<ref name="ref1" /><br />
<br />
Acute lymphoblastic leukemia (ALL)<ref name="ref2" /><br />
===Expression===<br />
-<br />
===Evolution===<br />
-<br />
===Sequence===<br />
>NR_149048.1 Homo sapiens LAMC1 antisense RNA 1 (LAMC1-AS1), long non-coding RNA<br />
<dnaseq>GTGGCACGATAACAGCTCACTATCACCTCAAACTCAAGTGATGCACCTGCTTCAGTCTCCCGGGTAGCTA<br />
GGACTACAGGCGTGTAGCACCACACCCAGCTAATTTTTAAAATAATTTGAAGAGACGAGATACTGCCAGC<br />
AAGATGAGTTAAGAAAAATCACTGTTTAGTTGTACAATGATACTGGACCATAAATGCTACCCTAGCTGGC<br />
AATATATCTTCAAAATATAAAAAGAAACTCCTCAGACCACAGTGTTCTACTTAGGGCAAGGTCCACAGAA<br />
GGCACCTAATGAAAATGACCCACACTGAGGGACTATGTTTTCTGGCAGCAGTGAACGACGGCCTCTTCTT<br />
TGCCACTGAAAGTGAGCAAGTAACCACAAGTTCGTGTATGTCATTACCGTGATTGCTACACCCAACTGGA<br />
AAAAGAATATTCCTACTGTGACTCCATTAAAGTCTTTTCAAAGCAAA</dnaseq><br />
<br />
==Labs working on this lncRNA==<br />
*Research Center for Medicine and Biology, Zunyi Medical University, Zunyi, Guizhou, China. <br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Gong J, Tian J, Lou J, et al. A functional polymorphism in lnc-LAMC2-1: 1 confers risk of colorectal cancer by affecting miRNA binding[J]. Carcinogenesis, 2016, 37(5): 443-451.<br />
</ref>(1)<br />
<ref name="ref2"><br />
Hashemi M, Bahari G, Naderi M, et al. Association of lnc-LAMC2-1: 1 rs2147578 and CASC8 rs10505477 polymorphisms with risk of childhood acute lymphoblastic leukemia[J]. Asian Pacific journal of cancer prevention: APJCP, 2016, 17(11): 4985.<br />
</ref>(2)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=SBF2-AS1&diff=1276495SBF2-AS12019-08-13T08:34:44Z<p>Qianpeng Li: </p>
<hr />
<div>==Annotation==<br />
===Name===<br />
Approved symbol: BF2-AS1<br />
<br />
Approved name: SBF2 antisense RNA 1<br />
<br />
HGNC ID: HGNC:27438<br />
<br />
EnsemblID: ENSG00000246273<br />
<br />
LncBook transcript ID: HSALNT0290236<br />
<br />
===Characteristics===<br />
-<br />
===Function===<br />
[[File:SBF2-AS1-fun.jpg|right|thumb|300px|The Schematic representation of NFAT5/SBF2-AS1/miR-338-3p/EGFL7 axis in GBM cell-driven angiogenesis<ref name="ref2" />.]]<br />
[[File:SBF2-AS1-exp.jpg|right|thumb|400px|Downregulation of SBF2-AS1 inhibited GBM cell-driven angiogenesis in vitro<ref name="ref2" />.]]<br />
<br />
*SBF2-AS1 is upregulated in non-small cell lung cancer (NSCLC) and promotes proliferation of NSCLC tumor cells. SBF2-AS1 may serve as a novel biomarker and potential therapeutic target for NSCLC patients<ref name="ref1" />.<br />
<br />
*knockdown of SBF2-AS1 repressed GBM cell-driven angiogenesis via enhancing the inhibitory effect of miR-338-3p on EGF like domain multiple 7 (EGFL7). In vivo study demonstrated that the combination of NFAT5 knockdown and SBF2-AS1 knockdown produced the smallest xenograft volume and the lowest microvessel density. NFAT5/SBF2-AS1/miR-338-3p/EGFL7 pathway may provide novel targets for glioma anti-angiogenic treatment<ref name="ref2" />.<br />
===Regulation===<br />
NFAT5 regulated SBF2-AS1 at transcriptional level, and SBF2-AS1 might be involved in NFAT5-mediated GBM cell-driven angiogenesis<ref name="ref2" />.<br />
===Diseases===<br />
Non-small cell lung cancer (NSCLC)<ref name="ref1" /> <br />
<br />
Glioblastoma (GBM)<ref name="ref2" /><br />
===Expression===<br />
SBF2-AS1 is upregulated in non-small cell lung cancer<ref name="ref1" />.<br />
<br />
SBF2-AS1 is upregulated in glioma samples<ref name="ref2" />.<br />
<br />
===Evolution===<br />
-<br />
===Sequence===<br />
>NR_036485.1 Homo sapiens SBF2 antisense RNA 1 (SBF2-AS1), long non-coding RNA<br />
<dnaseq>CAGGTTCCAGCCCCGACCCGGGCGCGCGGGGCCGACTAGGGTCGGGTCCAGTGTGCGGTGGTCGCTCCGC<br />
TCCGGGCCGCTCCGCTCTGGGCGTCAGGGCGCGGGGAGCTGCCCCGGGGTTCTGTCCACCGGGGAGGAAA<br />
GCCACGAGCACTGAGCGCCTCCTGAGAGCCAGCCCTGACGTGAACTCATTTTATCTGCCACGACCCAGAA<br />
GGAGTCTACTGCTAAGATTTCAGCATGTCCTGTGGCTGAGTTAATCAGAGTTATGACAGGAAGGTACCGG<br />
GCACACCATCGCAATGCTCCATCAATGCTAGTATGTTGTGTTCTTTCCTTCATATCAAGTCAACTCAAGC<br />
TTGCTCTACTTACCTGGTGTACACAGTCTAAGAACTGTAAGAAGACTGGAGCAAAACCACTCCCCTGACA<br />
GTTGAGGGTCAAGCTGCTCCTCTGACTGAATTTGTGACCAAAAGAGAGCCACTCTTTTTCAACCAACATC<br />
TGGAAGCCTTCAAGTGTCCTATAAAAGGGATCACTGAGTAACTGAACCAGGGATGTCACCTAGGGCATAA<br />
GCAGGATGGATTGTCATTAATTTTAGTTCTGAAAAAGGCCTATTACTAAGATAAAAGCACTTCCTTCTGA<br />
TGATAGCTAATTCACAAATTTACCTGGACAGCAAATTTGTTCACTAACCATTCCAGGATGGCCAATAAAA<br />
TTAATTTTGTAAACTTGCCAGTAAAAACTAAAGCTCAAATTCATTTTGGCTACAAGTTTACTTTCAGGGA<br />
ATTGAGACTTTAATCCTTAACTGGCCAGTTTGCTGACAGCAACCTTTTCCTAAGTTAATCAGAGGCCAGA<br />
GGATCAGTTAAAATCAATTCTACTTTTTGGCAGATGCAGATTAATGTCTTAATGTAGTCTGAACTCACAC<br />
TTTTCACTCTGGAGTGAGTTAAGGCGGGGCTTATAGAGAGCCAGGGGATGGACTGACAAAACCCAGGAAG<br />
GATGGTCCACGCCTCACACTGCTGGTCAAGGGCTCCATCCGCAAGCCTGCATGGTACATCTGTGGATGGG<br />
AGAGCTTGATGCCCGGAGCCAGAGCTCCAGGCTGCGTAGGGGCTAAGAGCTCATGGTACGGAGTTTTCTG<br />
ATGGATACCAGGTGCTGTTTAACACAGGACTTTCTCTGTCCATAAACACATTAGTCATTATACAAAAGAG<br />
TCATCTGAAGAATTTAAAAATGACCAAATGGAAATATAAATATAAAATATCAAAAAATATGTCTAATAGT<br />
TTACTTGTGCAGTGATGTCCCAGCCTTCCTCCAAACAGACCAAAACTGAGGAACCATTCTCAAGTACTTC<br />
TGATACAACCACAGCCAGCTGCATTATCCTGTGAAGCTAAGAGACAGGAAGGAGAACACAATTAGACCAA<br />
GCGCTTTCTGAGTGCAGAAGTCAGAGAGAGTTGCTTTCAACCCTGGATAATCAAACGACTTAGGGATAAA<br />
GCGCTTGCACAAAAGAACCACATAATGTTTTAAATACCTAAAGTTCTTTCAAATCAAGATTAAACAATGA<br />
CACTTTTGACTGGATGCAATGACTCATGCCCATAATCCCAGCACTTTGGGAGGCCGAGCCGGGCAGGTCA<br />
TTTGAGGTTCGGAGTTCGAGACCAGCCTGGGCAACATAAGCAAGACCCTGTCTCGAAAAATAAAAATAAA<br />
AAAGATACTCCTATTTGTCTATACTGTGTACTAAATGAGAAAAAAACTTTCAATATATTTGTGCTAAGTT<br />
TTTAAAGCCACATCAATTGGCTCAAAGTCCTTAATAAACAATTAAGGTATGAGAATAGTATATAGATTTT<br />
AAAACCAGATGTATAACATTGTAATTTTAAAAAATATTTTAATGATCATCAGACATAATTTGCAATTTGA<br />
ATCCAACTCTGAACAAGAACAAAAATGAAAAAACCCATCTCTTAAACAGAGCTAGGCTACTTTAAACACA<br />
GGAATAAGGCAAATGCCCTACTCAGTAATGAGAAGCTCCTCATGTAACTGTTTCTACAACATAGCTATCA<br />
CCAGGCCTGAATTCTTTTGGGCTCAGAATTTGTTCTAAGAAATGGCTATTATTAAAAAGTCAAAAAATAA<br />
CAGATGCTGGCGAGCCTGTGGAGAAAAGGGAATGTATATACATTTCTGGTGGGAATGTAAATTAGTTCAG<br />
CCATTGTAGAAAGTAGTTTGGTGATTTCTCAAATAACTTAAAACAGAATTACCATTTGACCTAGCAATCC<br />
CATTACTGAGTATATACCCAAAGGAATATAAATTGTTCTACCATAAAGTCACATGCACACACATGTTCAG<br />
TGCTGTACTATTCACAATAGCAAAGACATGGAGTCAACCTATATGCCCATCAACGGTAGACTGGATAAAG<br />
AAAATATGGTACATATACACCATGGAATACTACACAGCCATAAAAAGAATGAGCTTATGTCCTTTGCAGT<br />
AACACAGCTGAAGCAAACTAACACAGGAATGGAAAACCAAATACTGCATATTCTCACTTATAAGTGGGAG<br />
CTAAACATTGAGTACACATGGACACAAAGAAAGGAATAGACGCCTGGGGCGTATTTGAGGTTGGAGGTGA<br />
GAGGAGGGTGAGGATAGAAAAACTACCTATCAGGTACTATGCTTATTACCTGGGTGATGAAATAATCTGT<br />
ACACCAAACTCCCAAGATATGCAATGTACCTATACAACAAACCTACAT</dnaseq><br />
<br />
==Labs working on this lncRNA==<br />
*Department of Thoracic Surgery, Huai'an First People's Hospital, Nanjing Medical University, 6 West Beijing Rd, Huai'an, 223300, China.<br />
*Department of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, China.<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Lv J, Qiu M, Xia W, et al. High expression of long non-coding RNA SBF2-AS1 promotes proliferation in non-small cell lung cancer[J]. Journal of Experimental & Clinical Cancer Research, 2016, 35(1): 75.<br />
</ref>(1)<br />
<ref name="ref2"><br />
Yu H, Zheng J, Liu X, et al. Transcription factor NFAT5 promotes glioblastoma cell-driven angiogenesis via SBF2-AS1/miR-338-3p-mediated EGFL7 expression change[J]. Frontiers in molecular neuroscience, 2017, 10: 301.<br />
</ref>(2)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=LINC00628&diff=1276494LINC006282019-08-13T08:33:38Z<p>Qianpeng Li: </p>
<hr />
<div>==Annotated Information==<br />
===Name===<br />
<br />
Approved Symbol: LINC00628<br />
<br />
Approved Name: long intergenic non-protein coding RNA 628<br />
<br />
RefSeq ID: NR_027022<br />
<br />
LncBook transcript ID: HSALNT0020406<br />
<br />
Ensembl ID: ENSG00000280924<br />
===Chromosome===<br />
1q32.1<br />
<br />
===Characteristics===<br />
LncRNA LINC00628 locates in the second intron of PLEKHA6 (pleckstrin homology domain-containing A6) in chromosome 1q32.1, the mature RNA of which is 1290bp and has a poly-A tail and is discovered in many tumor formations<ref name="ref1" />.<br />
===Function===<br />
<br />
* The overexpression of LINC00628 inhibited the proliferation, invasion and migration and promoted cell apoptosis in osteosarcoma cells through the inactivation of PI3K/Akt signaling pathway<ref name="ref1" />.<br />
<br />
===Regulation===<br />
-<br />
===Diseases===<br />
Osteosarcom<ref name="ref1" />. <br />
<br />
===Expression===<br />
[[File:LINC00628-1.png|right|thumb|600px|LINC00628 expression was decreased in osteosarcoma tissues and associated with the metastasis and poor prognosis of cancer.<ref name="ref1" />.]]<br />
LINC00628 expression was decreased in osteosarcoma tissues and cell lines and associated with the metastasis and poor prognosis of cancer<ref name="ref1" />.<br />
{| class='wikitable' style="text-align:center"<br />
|-<br />
! | Experiment<br />
! | Forward primer<br />
! | Reverse primer<br />
|-<br />
| rowspan="1"|Quantitative real-time PCR<br />
| | 5'-AGAGCGAGCAGGATGAGATAGT- 3'<br />
| | 5'-GTGAGCAAGGAAGTTGACAGTG- 3'<ref name="ref1" /><br />
|}<br />
<br />
===Evolution===<br />
-<br />
===pubmed IDs===<br />
12477932, 30280767<br />
===Sequence===<br />
>gi|224282134|ref|NR_027022.1| Homo sapiens long intergenic non-protein coding RNA 628 (LINC00628), long non-coding RNA<br />
<dnaseq>AGCCAACTGGTTGTCTAAGGCTGGGAAGGGGTTAAGATGCCCCCGGAGCTTGCCGCGAGGGCAGCTGCCTCAGCGGGCACTCCGCCTGGATGGGAATATAAGCACTCTTGGTGTTGCCCAGGCAGAGAGGGCAGTGTGGAGGGAAGTTGCTAGAAAAAGGCAGGGGACATAATCCATACTGGCCTCTTTCCCAGGCACATCACAGTGGCAGAATTATTTATGATTCTGACCCAATGGGGATCCCTCTACTTGGGGAGACTGCCAACCCACGCCCTCCTGAATGGCAACGTCCTCCCACAGAGACAGAGGGGAACAAGTAGCATTTATGGAGCGGCACAGAGGAAAGAGTGTGGGCTTTGGAGACAGCACAGCAGCACTCACATCCCGGCCCAGACACTTCCTGTGTGACCTTGAGCCAGTTGATGAACCTGTCTGGGCCTCTGTTTCCTCATCTGTTATCGGCGAAAATGTTTCGGAGGACACCTATTGTATAATGTTGCTATGCAGATTAAATGCACTAGCAGAGGCAAAGTGCATAGCTTAGAGGAAGGAAGTACTCGCTAAGTGGTAGCTGGTGTGATAGGTGGGCCAAGTCCTGGCAGGAGCTGGGCTTGCTGGCTGCCCTGTTTTGCTGAAACAGCAGCATCACCATCAGCAGCAACTGTGGAAATATAGACCCTTGATAAATACAGGTGAATAAAATGAATGATTAGAAACTGGACCTGCCACTCTGCAGAACCCAGGCACTGCTCCCCAGCAGCTGGTGCCTCAAAGCAGCTGCTAACATGGCAGGAGACAGTCAGACCAGCAGTGAATAGCTATGCTTCGTAAGACTTCATACACAAGGCAGGCGTGTGGACTGACCAGAAAGGTGGCAGTCACTGTCCATCAAGAGAATCCCCACCTGTTTTCCAATATGTCAGCCAGGAGGCTCGCACTCCCAAAAGGAATGTTCTCAGCCAGCTCCCTGACTGTCCCCACCTCTGACAGTGGACTCTCTTGGGTCTCTCAAAAGGCTCCTCCTCCTCAGCCATGGGGTGAAGGAATCCTGTTTGCCGGGGAGGCGGGATGCTGCCCAGGGTGGCTGTTTTGGGAGAGCGAGCAGGATGAGATAGTGCCTATGAGTGATCTTTGGAGATGGAGGTGCTATGGCCACCTGTGGGGACTGCCTGGGTGCCTCCTGGCCACTGTCAACTTCCTTGCTCACACTGAGATTCTGTGATTCTCCTCTGAGCATTTCCATGGATAATTTTTTTTTTTCAGAGACACTATTAAAGATTTTAAAAATTG</dnaseq><br />
<br />
==Labs working on this lncRNA==<br />
* Center for Joint Surgery, Southwest Hospital, Third Military Medical University, Chongqing (Army Medical University), China. jointsurgury@163.com.<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
He R, Wu JX, Zhang Y, Che H, Yang L. LncRNA LINC00628 overexpression inhibits the growth and invasion through regulating PI3K/Akt signaling pathway in osteosarcoma. Eur Rev Med Pharmacol Sci. 2018 Sep;22(18):5857-5866.<br />
</ref>(1)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=LINC01138&diff=1276493LINC011382019-08-13T08:32:57Z<p>Qianpeng Li: </p>
<hr />
<div>==Annotated Information==<br />
===Approved Symbol===<br />
[[File:LINC01138-1.png|right|thumb|400px|LINC01138 is associated with clinical outcomes in patients with HCC<ref name="ref2" />.]]<br />
[[File:LINC01138-2.png|right|thumb|400px|Integrated model depicting lncRNA LINC01138 as an oncogene in liver cancer<ref name="ref2" />.]]<br />
LINC01138 (long intergenic non-protein coding RNA 1138)<br />
===Previous Symbols===<br />
LINC00875<br />
===Synonyms===<br />
FLJ39739<br />
===Chromosome===<br />
1q21.2<br />
===RefSeq(supplied by NCBI)===<br />
NR_027468<br />
===LncBook transcript ID===<br />
HSALNT0014603<br />
<br />
===Characteristics===<br />
-<br />
===Function===<br />
*The high level of LINC01138 is correlated with a short biochemical recurrence-free survival times.<ref name="ref1" /><br />
LINC01138 promotes the proliferation and inhibited apoptosis of PCa.<ref name="ref1" /><br />
LINC01138 functions as an oncogenes in prostate cancer.<ref name="ref1" /><br />
<br />
*LINC01138 is associated with the malignant features and poor outcomes of HCC patients. LINC01138 acts as an oncogenic driver that promotes cell proliferation, tumorigenicity, tumour invasion and metastasis by physically interacting with arginine methyltransferase 5 (PRMT5) and enhancing its protein stability by blocking ubiquitin/proteasome-dependent degradation in hepatocellular carcinoma (HCC)<ref name="ref2" />.<br />
<br />
===Regulation===<br />
The LINC01138 transcript is stabilized by insulin-like growth factor-2 mRNA-binding proteins 1/3 (IGF2BP1/IGF2BP3)<ref name="ref2" />.<br />
===Disease=== <br />
Prostate cancer<br />
<br />
Hepatocellular carcinoma (HCC)<ref name="ref2" /><br />
===Expression===<br />
<br />
The expression level of LINC01138 is markedly increased in invasive extraprostatic tumors (pT3a, pT3b and T4 stages) as compared with intraprostatic localized tumors (pT2a , pT2b and pT2c stages).<ref name="ref1" /><br />
<br />
The LINC01138 locus is frequently amplified in hepatocellular carcinoma (HCC)<ref name="ref2" />.<br />
===Sequence===<br />
NR_027468.3 Homo sapiens long intergenic non-protein coding RNA 1138 (LINC01138), transcript variant 1, long non-coding RNA<br />
<dnaseq>AGCTGGGCGGTCACATCTGGAAATGGAAAGCCGACCTCCCCCTCCTCCTCCACCTCCTCCTCCTCCTCCT<br />
CCTTCTCCTCCTCTCACCCAGGATCACTTCCGAAACCAGTTGGCCTTCAGCCCCTGCCTCGGCCAGAGGT<br />
TTCATTTTTAACTGAATATTTACGAAAGCTGAAAGCGTGCGAGGGGGGTGGGGTGGAAATAGCGGCTGCT<br />
TCTTTTCCAAGGATTTATTTAATGGGGATGTGTTCAAGGCAAGACCGAATTCAGAAGGATATCGACGTCG<br />
TGATCCAGAAGTCCAGAGCTGAGGACTGCCTGTTTGCAGTTCTGTTTCATCAAATGGAAATGGGACATGG<br />
ACAGTTTCTCCTATCCCATGCAGACCATGCTCCTGAATTAAAACTGCAGAATGTGTTAAAGCATCATTCA<br />
ACATCGTGAGCACATTTGAGATACTGTACAGGACAACCTGCTTTTCATATTCTCTGTGAATTTCAAAGAC<br />
GACTGGGATTTTCTTCCTCCTCTACCACCCTGAACAGCAAGACCAATACATCCTGTATTTCCTCCTCTTC<br />
AGCCTACTTGTGAAGACAAGGATGAAGACCTCCATGATGAGCCATCTCCACTTAATGACTGTCTCACATT<br />
GGCCGGCAACTTGTTCCAGATGAAATCTTGCTCTGTCACCCAGGCTGGAGTGCAATGGCTCGATCTCGGC<br />
TCACTGCAACCTCCACCTTCTGGGTTCAAGCAATTCTCCTGCCTCAGCCTCCTGAGTAGCTGGGATTACA<br />
GATGGAGTCTCACTGTGTCCCCAGGCTGGAGTGCAGTGGCGCGATCTCAACTCACTGCAAGCTCTGCCTC<br />
CCGGGTTCACGCCATTCTCCTGCCTCAGGCTCCCGAGTAGCTGGGACTACAGGCGCCCGCCACCACTCCC<br />
GGCTAATTTTTTTTGTATTTTCAGTAGAGACGGGATATCACCATGTTAGCCAGGATGGTCTCGATCTCCT<br />
GACCTCGTGATCCGCCCTCCTCAGTCTCCCAAAGTATTAGGATTACAGGCGTGAGCCACCGCCCCCGGCC<br />
CTCAAAGATTGTTATGAGTCCTCACAGATGTCAGAGGACGATGCTGTGACCTATATTTGCAAACGCCCGG<br />
AAGACTTAAAGCTATTGTTTTGCAAATGCACAGATAACAATAATAACATGATGCTGTGGATGAGCATGAA<br />
AGTTTTTCTCTTACTCCTAATTATAATGTTTTCCCTCTTACTGCTTTGCCCTGCTGATGGAATTCAGTAA<br />
AGGAATCTCTACCAGCAGACACTTGGTTTTTACCCTTCCTAGGACCTTTAATAGATATCTTTTTATTACT<br />
AATCTTTGCTCTTTGCTTGTTTAACCTCCTTGTAAAGTTTGTGTCTTCCAGATTACAATAATTCCATGTA<br />
AAGATGATGCTGGCACAAGGCTTTCAACCCATCCCCTCTTCTGACCCAGAAGATAAAGACATCCTACCTT<br />
TGAGCCTTTTAGAACAGGTATCCAGGGATTTTACCTCTCCAGTGCTAGGCAGGGTCTATGCCCATAACAT<br />
CAGCAGGAAGCAGTTACAGAAGATGAACCTCCGCCCTTCTGCAAGCCCCTTAAGATTAAGGAGGAGTATA<br />
TAATCTCTGATGGGGAAATGAGGTAGGAGACCAGAAGGACTTATTTTCCATTCCCAACCCCATTGAACAG<br />
AGCAGGATCTGGTCAAAACAGGGTGCAGTGGAGAAGCCTGCTGAAACCAGCAGATGATGATGAAAGTGAC<br />
CTCTAGTTGCCCTCACTGCTTATGAGCATAAAGACACTACCACTGGGACCATGGCCAGTTTACAAATGTC<br />
ATGGCAACACACCTTGGCAATGGCCTGGAAGTTACTTTATATGGTTCTGGAAACTCCCTGCCCCTTTCCC<br />
AGAAAGTTCTGAATAACCTACCTCTTAATTGGCATGCAATTAAAAGTGGCTCTAAATACAACTAGCTAGT<br />
AGCCCACAGGCACAAACTCTGGGCACACTGCCTATAGGTTAGCCCTGCTCTGCAAGAAGTAGCACCAGTT<br />
CAATAAAAGTTGCTTTCTCTCAAAAAAAAAAAAAAAAAAAAAAAA</dnaseq><br />
<br />
==Labs working on this lncRNA==<br />
* State Key Laboratory of Genetic Engineering, Shanghai Engineering Research Center Of Industrial Microorganisms, School of Life Science, Fudan University, Shanghai 200433, PR China.<br />
* Fudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China.<br />
<br />
==References==<br />
<references><br />
<ref name="ref1">Wan, X., et al., Identification of androgen-responsive lncRNAs as diagnostic and prognostic markers for prostate cancer. Oncotarget, 2016. 7(37): p. 60503-60518.<br />
</ref>(1)<br />
<ref name="ref2"><br />
Li Z, Zhang J, Liu X, et al. The LINC01138 drives malignancies via activating arginine methyltransferase 5 in hepatocellular carcinoma. Nature communications, 2018, 9(1): 1572.<br />
</ref>(2)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=LINC00598&diff=1276492LINC005982019-08-13T08:32:04Z<p>Qianpeng Li: </p>
<hr />
<div>==Annotated Information==<br />
===Name===<br />
Approved Symbol: LINC00598<br />
<br />
Approved Name: long intergenic non-protein coding RNA 598<br />
<br />
Previous Symbols: -<br />
<br />
Synonyms: TTL, lncFOXO1<br />
<br />
RefSeq ID: NR_024505<br />
<br />
Ensembl ID: ENSG00000215483<br />
<br />
LncBook transcript ID: HSALNT0200443<br />
===Chromosome===<br />
13q14.11<br />
[[File:Lncfoxo1-fun.png|right|thumb|400px|Overexpression of lncFOXO1 inhibits cell proliferation, colony formation, and induces G0/G1 cell cycle arrest and apoptosis in breast cancer cells<ref name="ref1" />.]]<br />
<br />
[[File:Lncfoxo1-exp.png|right|thumb|400px|Downregulation of lncFOXO1 expression in human breast cancer tissues<ref name="ref1" />.]]<br />
===Characteristics===<br />
A total length of 683 nt of lncFOXO1 transcript was determined by a RACE assay. LncFOXO1 was mainly localized in the nuclei of breast cancer cells <ref name="ref1" />. <br />
===Function===<br />
<br />
<br />
* LncFOXO1 suppresses the growth of human breast cancer cells through association with BAP1. Mechanistically, lncFOXO1 suppressed the growth of breast cancer by increasing FOXO1 transcription. Moreover,lncFOXO1 associated with BRCA-1-associated protein 1 (BAP1) and regulates its binding and the level of mono-ubiquitinated H2A at K119 (ubH2AK119) at FOXO1 promoter<ref name="ref1" />.<br />
<br />
===Regulation===<br />
-<br />
===Diseases===<br />
Breast cancer<ref name="ref1" />.<br />
<br />
===Expression===<br />
lncFOXO1 is significantly decreased in breast cancer tissues and cell lines and downregulation of lncFOXO1 expression associates with poorer overall survival<ref name="ref1" />.<br />
<br />
{| class='wikitable' style="text-align:center"<br />
|-<br />
! | Experiment<br />
! | Forward primer<br />
! | Reverse primer<br />
|-<br />
| rowspan="1"|Quantitative real-time PCR<br />
| | 5'-CGATGTGCTGGAGTGTATGT- 3'<br />
| | 5'-GCAGGATGGCACTACTGATAA- 3'<ref name="ref1" /><br />
|}<br />
<br />
===Evolution===<br />
-<br />
===pubmed IDs===<br />
12764377, 28339037<br />
===Sequence===<br />
>gi|213688418|ref|NR_024505.1| Homo sapiens long intergenic non-protein coding RNA 598 (LINC00598), transcript variant TTL-T, long non-coding RNA<br />
<dnaseq>CGCTGTAGAGCTCCGATGATGGCTGTTGGCCGAATGGATGAATGGCTTCATTAACTTCACTGCAACACGCAGGAGTCCTTGATCTCCCCCCTTGAAAGGCTGGAGCACAGTGGCATGATCTCGGCTAACTGCAACCTCTGCCTGCCTCCCAGGTTCAAGCAATTCTCCTGCCTCAGCCTCCCAAGTAGCTGGGATTACAGCAAACAATGGACTATTGACTAAGCTTTCAGAGCTGTGGGTGTTCTCAGAGGGAGGCCAGCCAGAACACCAGCATCTCCGGCTTTTCTTCCAACTCCCAAGTTGGAGCTCCATCTATCAGAAATATGAAACCCTGGAATCTTCCTCCTCCTCACTTCTCTGCCTTAAGATCCTAGTCCACTGCCTGGAACATGGAAGATGCTCCATAATTGTTTGCTGAAGGAACGAGTGATAACCAGAGAAGCCAGCTCCTGCTTCCTGATTAAGGCATGCAGTCAGGCCAGTGGGGAAATGGGCCTCATGGTGGAGCTTGCCTCTGCTGGAAGACTGACGGAGCCAGGGCTCTGCCTGCCACAATTCATGAGCTGGCCAGAGGTCTTTGGATTCCTCCCAGTCATTGCTGAGATGAGTGAGGATTGTTTCAGAAAATCAGGCCTCCTCCTGGGGAATGTGCCTCAGCTTCTGGCTGCATCAGTGATTTGGACACCCCTTAAGGACAAAGAGCGTGGTTGGGAGAAGAGCGCTTTCCACCCCTCTCCTTCAGGACCATCCTGGATGCAGCTGCAACTCTGCTCTTGGCTGTCCTATGGCTGGCAATAGCTTTCTTGCTCTCTGGCAGGCAAAAAGCAGGGTGTGTGTGTGTGTGTGTGCATGCGTGCACGTGCTCATGTGTGCATGCACTGGAAAGCTAAGGCTGAGGCATCGAATGACAAGATCCCTGAAGTAAAAGGCTCCACAGCTGCTTACCCAACCCCTAATTTGCTGGGGCTGGGCTCCTTCTAATGGGCTGCCAGACCCTGGTAGGCACAAGGAGACTGGCTGTATATGTCTCGTGTCCCCTGGGCGACTGTCCCAGTGAGCAAGGACACCACCAACCTTCTTCCCCCCTACACCCTCCATAGGACAGTGAGATCCTGCATTGGATTATGCATGAGGTGTATACACTCTGCTTGTACGTATGTATGGAAGAAAGGATTTTGGCTTGAAACATTTTTTTTATTGGCAGAGACAGCACTTCTCTTAAAGGAAATGGCGGAATTTGCCAAACTAAGCCTCCAGAAGAAAATATAACGGAGAGTGTAAAAGAAATCCATGTTCAAACATTGGCAAGTGTGAAACATTCAAGATTTTTGTGTGAACATCACATTGTGGGAGCAAAATTAAATTAAGCTGGTCTCTGGCAAGCATTGGAATGAAAGCAGAACTGGAGCAAGCGGATGGTGCTTGGGCATTTTTTGCAAGAAGCCAAACAGAGCATAATCAGATGACAACCAGGGATCCCAAGGGCTGGGTTCTTTTCTTCATCTCATTAACACACAAGAACTTAACTGCTTTGGGTCCGGAGGGTCCCAAGGAAGTGCCAAAAGAACCTGAACTTTCTTCACCTCCACAACTCAATGACAGGCAGAGAAGGAATGAATTTCATTCAAAAAATATTTATTGAGCATCCTCAGAATATTTATTGTGCAAACTACTGTTCCAGGCACCAAAGGAGGGGATGGTCCCAGCTCCTTTATGGAGTCTGCAGTCCACAGACTTGAACTCAACTAACTAGAAGGAAAGGCAGCTCAGAGCAAGTGCCCTGCTGGAGATTGAAGCAAAGTGCCAGAGAACGTGGGGGTCATTCAAGAATGAGGTTGGAAGAGATCATTCTCCTGTTTGCAAATGAGAAACAAGTATAGGTGTGAAGAGACCTGTCCACAGCCATTCAACAAATGAAAAGTCCAATCGAAGATGGGACCTGATTTCTTACACCCCAGGTATCTGCTCATCATCTTGGGTAAGACCACAGGGACCACCAAGACACCCAGAAGAGACACTTGATTGTTTCCTGGATGTTCCAGTTTTGGGGCCCATAGATATATGCCATTTACTTTACATGCTTTCTAAAAAA</dnaseq><br />
==Labs working on this lncRNA==<br />
* Department of Gynecology, Cangzhou Central Hospital, Cangzhou, Heibei 061001, P.R. China.<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Xi J, Feng J, Li Q, Li X, Zeng S. The long non-coding RNA lncFOXO1 suppresses growth of human breast cancer cells through association with BAP1. Int J Oncol. 2017 May;50(5):1663-1670.<br />
</ref>(1)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=LINC00460&diff=1276491LINC004602019-08-13T07:58:23Z<p>Qianpeng Li: </p>
<hr />
<div>==Annotated Information==<br />
===Name===<br />
Approved Symbol: LINC00460<br />
<br />
Approved Name: long intergenic non-protein coding RNA 460<br />
<br />
RefSeq ID: NR_034119<br />
<br />
LncBook transcript ID: HSALNT0289038<br />
<br />
EnsemblID: ENSG00000233532<br />
<br />
===Chromosome===<br />
13q33.2<br />
<br />
===Characteristics===<br />
-<br />
===Function===<br />
<br />
* Loss-of-function assays showed that LINC00460 knockdown significantly suppressed the proliferation ability, increased the apoptosis and decreased the proteins (MMP-2, MMP-9, ZEB1) expression. LINC00460 promotes MMP-9 expression through targeting miR-539, acting as an oncogenic RNA in the meningioma malignancy and accelerating the proliferation and metastasis of meningeoma<ref name="ref2" />.<br />
<br />
===Regulation===<br />
-<br />
===Diseases===<br />
Colorectal cancer<ref name="ref1" />. <br />
<br />
Meningeoma<ref name="ref2" />.<br />
===Expression===<br />
[[File:LINC00460-exp.png|right|thumb|400px|LncRNA LINC00460 was over-expressed<br />
in meningeoma tissue and cells<ref name="ref2" />.]]<br />
LINC00460 expression level was significantly up-regulated in meningeoma tissues<br />
and malignant meningioma cell lines (IOMM-Lee, CH157-MN)<ref name="ref2" />.<br />
<br />
{| class='wikitable' style="text-align:center"<br />
|-<br />
! | Experiment<br />
! | Forward primer<br />
! | Reverse primer<br />
|-<br />
| rowspan="1"|Quantitative real-time PCR<br />
| | 5'-AATGGTGGTAGGAGGGAGGA- 3'<br />
| | 5'-CAAGGGGAATGAACACGAGG- 3'<ref name="ref2" /><br />
|}<br />
<br />
===Evolution===<br />
-<br />
===pubmed IDs===<br />
27591862, 29906745 <br />
<br />
===Sequence===<br />
>NR_034119.2 Homo sapiens long intergenic non-protein coding RNA 460 (LINC00460), transcript variant 1, long non-coding RNA<br />
<dnaseq>CTTCCTGCAGAAATCCTCCAGCCCTGTTAGAAATGCCTCAGCCAGGGGGACTCATCTCCTCAAACCTGGG<br />
GGACCGAGACCTATGAGAGGTCACAGCATGAGCCAGGACATCGGAGGTACCCAGACATTGTTATGAAACT<br />
CCGCATGTGCCCCTGGTGGACGCTGCTGGACCCAGCATGCACACTTCTCGGCTAAGAGTCACCCTGGATG<br />
AACCACCATTGCCAGCGGGGAGCATGTTGCAGCTTTCCCACGCAGTGGATGAGAACGAAGGTTACGACCA<br />
TTGTGTGGGAGGCGTCTGTGTAGCAATTGCTGGAATCACTTGTGGCATTGTAGAAAGACTGAGCGTGGGA<br />
AAGAAGACGCATTCTGAAGTCACCCCGATTTATGTTAAATTATCACCTTGACTACTGCTATAGAACGAAT<br />
GTTTATGTCCCCCACCCAAATTCGTATGCTAAGACCTAATAGCCAATAAGATAGTATTAATAGATGGGGC<br />
CTTTGGGAGGTGAGTGGCTCATGAGGGCAGAGTCCTCAAAACCAGATAAGTGCCCGAATAAAAGGGGCCC<br />
CAGAGAGATCCCTTGCACCGTCTACCATGTGAAGTGTAGAACACAGCGAGAAGGCCACCTATGAGCCAGA<br />
ACGTGGGCCCTCACCAGAACCCAGTTGTGCTGGCACCCTGATCCTGGACTTCCAGCCTCCAAAATGACGA<br />
CAAAGAAGTTTGTTTTTCCTGAGCCATCCACTTCAAAGTATTCTGTCATAGCTCCCCAAATAGACTAAGA<br />
CATCTACTTAACCTTGGTCAAACGTTTAACCTTGGAGTCCACGCCTCTGAAATGGTGACAATAACACTGT<br />
GTATTTCCTACTTTATGATCAGGATTAATAAATGTAATTTATTAATCAGAAATTAGTAATTTCTGATTAT<br />
TAA</dnaseq><br />
<br />
<br />
==Labs working on this lncRNA==<br />
* Qingdao University, Qingdao, Shandong, 266003, China.<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Wang R, Du L, Yang X, Jiang X, Duan W, Yan S, Xie Y, Zhu Y, Wang Q, Wang L, Yang Y, Wang C. Identification of long noncoding RNAs as potential novel diagnosis and prognosis biomarkers in colorectal cancer. J Cancer Res Clin Oncol. 2016 Nov;142(11):2291-301.<br />
</ref>(1)<br />
<ref name="ref2"><br />
Xing, H., Wang, S., Li, Q., Ma, Y., & Sun, P. Long noncoding RNA LINC00460 targets miR-539/MMP-9 to promote meningioma progression and metastasis. Biomed Pharmacother. 2018 Sep;105:677-682.<br />
</ref>(2)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=CPS1-IT1&diff=1276490CPS1-IT12019-08-13T07:57:28Z<p>Qianpeng Li: </p>
<hr />
<div>==Annotated Information==<br />
===Name===<br />
Approved Symbol: CPS1-IT1<br />
<br />
Approved Name: CPS1 intronic transcript 1<br />
<br />
Previous Symbols: CPS1IT<br />
<br />
Synonyms: PRO0132, CPS1-IT<br />
<br />
RefSeq ID: NR_002763<br />
<br />
Ensembl ID: ENSG00000280837<br />
<br />
LncBook transcript ID: HSALNT0046602<br />
===Chromosome===<br />
2q34<br />
<br />
===Characteristics===<br />
-<br />
===Function===<br />
[[File:CPS1-IT1-fun.png|right|thumb|400px|Overexpression of CPS1-IT1 inhibited cell proliferation in colorectal carcinoma cell lines<ref name="ref1" />.]]<br />
*CPS1-IT1 significantly reduced cell proliferation, migration and invasion capacities and accelerated cell apoptosis, thereby suppressing epithelial-mesenchymal transition (EMT). An in vivo animal model also demonstrated the tumor-suppressive role of CPS1-IT1.<ref name="ref1" />.<br />
<br />
===Regulation===<br />
-<br />
===Diseases===<br />
Colorectal carcinoma(CRC)<ref name="ref1" />. <br />
<br />
===Expression===<br />
[[File:CPS1-IT1-exp.png|right|thumb|400px|Relative expression of CPS1-IT1 in human colorectal carcinoma and adjacent non-cancerous normal tissues as well as in different colorectal carcinoma cell lines of varying metastatic potential<ref name="ref1" />.]]<br />
Expression of<br />
CPS1-IT1 was significantly decreased in CRC tissues and cell lines, and patients with low CPS1-IT1 expression had poor survival outcomes.<ref name="ref1" />.<br />
<br />
{| class='wikitable' style="text-align:center"<br />
|-<br />
! | Experiment<br />
! | Forward primer<br />
! | Reverse primer<br />
|-<br />
| rowspan="1"|Quantitative real-time PCR<br />
| | 5'-CAC AGA TGA TCC ACG GCG TT- 3'<br />
| | 5'-GCG TGC ATC AAT GAC ACT TCA- 3'<ref name="ref1" /><br />
|}<br />
<br />
===Evolution===<br />
-<br />
===pubmed IDs===<br />
12477932, 29145177<br />
===Sequence===<br />
>gi|192807280|ref|NR_002763.2| Homo sapiens CPS1 intronic transcript 1 (CPS1-IT1), long non-coding RNA<br />
<dnaseq>AATAAAACACTTGCTTTTCTTTTTGAGAAAAATTAGGTTCTTTTTCATCTATTTAATTATTGCCCATGTCAAATGCTTGGTTTTGAAAACTGAGGAATTCTATCTGACAAAGATGAAACCAGCTATAGTTGCTTGTAAATCATCCTTTCTAGTGATCACATAAAATGAACAGTAGACAGCAAATAATTTAGGAATTGAACCTATACATTTATCTTATAATTTTGCTGACTTAAGTTTCCCTTTCTTGGTTTATGATGCCAGCAGAACTTCTGTGTAAAATTATAGTCTGTTCTACTGTTCTCAGTTTCAGGCAACTGATTTCAAATGCCTATGAAACCACTCCAATTAAGCCACATGGGGGTGCTAGAAACTTATAGTATGCCAGTCACAGCAGTGGAAAAGACCTGGGGTGGAAAATAGCAGATGTTATTGTGATTTAAATTTCCACTTGACATACGTTCTGATTTTTGGACAAATTCAATGTTTTAATTGAATAGTTTTCGTTACAACCAGAAGGCAGGTTGAGATTCTAACTAAGCATAAATAAGGGTATATTGATAGTGAAAAAGGTCCTTGGAGGATTAAAACAACACACTGTTACAGATCATTTATAATATTTTTCTGACTTCCACATTCTGTTGCATTTATTTGCCGACAATTTGACATTTTCAATCTCCATTTTCTGGCATAAATATATTTGTAAATAGGGATATTTTCTATTGTTCATAATGATCTACATTTAAAACTCTTTATGTAAAGCTTTATATCATTTCAAAAATTTCAAAAACTTACACTTAAAATCATCTCTACTGTATAAATTTGTTTTTGATCCAGGGAGGTTGAAGTGTCTATTATATAGCAAAAGCTAAAGTAAACCTGAAGTGGAACTCACAGATGATCCACGGCGTTAGCAAACCTAAACCCTGAACTCATTATCTGAGTGTCACTTTATGGTTTAATTCCTTTCTTTTTGAAGTGTCATTGATGCACGCATAGCAATTTGATAATGATTGTTATTTAGCGGTATTAGATAAATAACAAGAATAGATGGCCACTAAAGCTACCTGTCTCCATCATTTTGTGGCACATAGGGGTCTGAAGTTGAAAGAATACGACAGCTGATGGAATGAATGTTAAGTATGTAAGGCCTTGAGTTTCCTTGCCCTATTTTAATTATACTCACCATTAGTCTGGGTCTGAGTCCTCTGCTTTTTCTCGGCCCCTCAATATCCAGGGAGGCTTAGTCATCAAGGTACGTACTGCTCCAACAGTAACAAGAGCTCCCTATTAATGACCTATAGCTGACTTACATATTGCGAGTTTGGAGAGAGGCTGAGAAGATTAGTTGTTCTTTTTCATTTGTATTTATTTATGGTTTACTTTGAAGATCTCAACTGCTTCTGTGTTAGAATGGCTGTCTTTAGCTGTAGGCCTAGGAGCTAGCGATTTATTTGGTGTGCGTTCAGAGAACTCCAAAATTCTCCTGCCTCAACATCTATCTCTGCTGCCAATGTACCGCACTCCCTTTGTACTTTTCATAGAGATCCTTGAGAAGACAGGCAGTGGGGCTCTCACTTGGGAAAAGAGAAGTAAATTAAGAGAAAAAATATAGAATGCTAGACGTGGGTTTTCTGGTTCCACCCTTGTGCATTGGAAGGAGCAGACTATGGAGCCAGAGATTGGTGCGCAGTCCTCCCCACTGTAGAATCAGACGTACATCACCTCTTTCATTTCTCCAGATTCATGTTCTTTCTCTTAATCTCTGCTTCTAGTTTTTTTGTGAAGCTTAATTTATATAAGTATAAATGACATCTGACATATTGTGAGGGCCCAAGAAAATTTTTCCTCTTTTCCCCTGAAAATAAAAATGCTACTTGTTGTAATAAAGGTTACTTTATGATTTTAGATATGTATTATATATTATGATTTTAGATATGTAGATATGATAGTTAAATATTTAAAGATTCATTTTCAGACTCACAATTTTTATTTGCTTTTATATTTTGCAATGTATCATTTCTTAATTTCCTTTATGATGCATCACTTATTTTAATATCAGACCTATTTTTTAAAGGAAGCAATTGATAGCTACGATGCAAATGCTATTCTTATTAAAAGATAAATAGCTTTCCCTTATGCTAATGAATAAAAATTCCTACTCTACAGTTGTTAATCAATCTCGAGTTCTAAAGTCCGATAAACACATTTAATAGCAGAGGATGAGCATATCATTAAATTGATGGTCAGTCTCTGACTTGTGTTTACATATAGTCATCTGAAATGAAGTTCAGAATTTGAGTCCCAAA</dnaseq><br />
<br />
<br />
==Labs working on this lncRNA==<br />
* Department of Colorectal and Anal Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Zhang W, Yuan W, Song J, Wang S, Gu X. LncRna CPS1-IT1 Suppresses Cell Proliferation, Invasion and Metastasis in Colorectal Cancer. Cell Physiol Biochem. 2017;44(2):567-580. <br />
</ref>(1)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=SLC7A11-AS1&diff=1276489SLC7A11-AS12019-08-13T07:56:03Z<p>Qianpeng Li: </p>
<hr />
<div>==Annotated Information==<br />
[[File:SLC7A11-AS1-1.png|right|thumb|400px|The role of the SLC7A11-AS1–SC7A11 model interacts in tumor development<ref name="ref1" />.]]<br />
[[File:SLC7A11-AS1-2.png|right|thumb|400px|SLC7A11-AS1 expression levels were assessed in human gastric cancer tissues and PBMCs<ref name="ref1" />.]]<br />
===Name===<br />
Approved Symbol: SLC7A11-AS1<br />
<br />
Approved Name: SLC7A11 antisense RNA 1<br />
<br />
Synonyms: ENST00000512786<br />
<br />
Chromosome:4q28.3<br />
<br />
RefSeq ID: NR_038380<br />
<br />
LncBook transcript ID: HSALNT0078323<br />
<br />
===Characteristics===<br />
-<br />
===Function===<br />
<br />
* SLC7A11-AS1, antisense to SLC7A11, could promote tumor growth in vitro and in vivo. The effects of SLC7A11-AS1 depend on the regulation of SLC7A11 via the ASK1-p38MAPK/JNK signaling pathway<ref name="ref1" />.<br />
<br />
===Regulation===<br />
-<br />
===Diseases===<br />
Gastric Cancer<ref name="ref1" />. <br />
<br />
===Expression===<br />
<br />
SLC7A11-AS1 is significantly down-regulated in gastric cancer <ref name="ref1" />.<br />
<br />
===Evolution===<br />
-<br />
===pubmed IDs===<br />
27816668, 29348845<br />
<br />
===Sequence===<br />
>NR_038380.1 Homo sapiens SLC7A11 antisense RNA 1 (SLC7A11-AS1), long non-coding RNA<br />
<dnaseq>TCTGTCTGGCAAGCGCCGCGCGCATCCTCGGTTCCCGCCGCGCCGTTGCCGCCGCTCCTCTCCCTCCTCA<br />
CCTCCCCGCAAGCTGAGGGAGCCGGCTCTGGCCTTGGCCAGCCCAGAAAGGGGCTCCCACAGTGCAGCGG<br />
TGAGCTGAAGGGTTCCTCAAGCGCGGCCAGAGTGGGCGCCAAGGCCGAGGAGGCGCCCAGAGCCAGCGAG<br />
GGCTGCCAGCAAGCTGTCACCTCTCAATAGGAACTGGTACCAACCTACTTACGAAGAAGTATTTGTTTTA<br />
ACCTGAACCTGGGGGAAAAACAACATGAACTGTTCGTCTATCTATATCGTCATTATTTTTTACCTCATGG<br />
ATTGAAACAAATTTTAAAGGAAAAAAGAATGTTAAGAAAGAGCAGCACTTACTATCAGGGAGGCACCTCA<br />
CGAGCATTGTAAACACTCAGGCTCGCTGCTTTCTGAAGGACATGCCAATCATGCACAGCACTTACTAGAA<br />
ACTGCAAGACTGCACAACATGATGGTATTTATTCCAGGAACAGGAGCCAGTCCTGGGCACACACATAAAG<br />
GGACTTCCTTCACTCCCCAGAAGAAGAGAAAGCATGCTGACACACATCTGCCCAAGCAATCAGAAGGCAG<br />
CTAAAGCCGCCACAGTCTTCACTCACCAACAGTTAGACCTTTTCAATTGATTTTATTGAAGAAAGTGAGT<br />
GCTGAGCACCATGAGTTCTCATAAACAATCCATTTTGGCAAATGCTTTAAGAATGTTGGTTAATTGCAGT<br />
TAGGCAGCATCGACGTATTTTATTTTTTGGAAAGCAAGAAGCTGGCTTACCAACATTAAGTTAAACAACA<br />
TGTAAGGGTTAGAAATATGAATCAACAAACTATTAGGGTGGTACCATCTCTTTATAATAAAACAATGTAG<br />
ATTGATTAAGTATAGCCTAAAAGTTTACCACAAATCATAACTACATTTAAGCTTTGAATTTCATGACTAG<br />
TGATTAATTTTGCATGTCAACTTGACTGAGCTTATAGAATGCCCAGGTATCTGATTAAACGTTATTTCTG<br />
GAGGTGTCTGTGAGGGTGTTTCTGTAAGAGATTAGCATCTGAAGGCCAGGTGTGGTGGCTCATGCCTGTA<br />
ATCCTAGTACTTTGGGAGGCCGAGGTGGGCAGATTGCCTGAGCTCAGGAGTCTGAGACCAGCCTGGGCAA<br />
CATGGCAAAACACCGTCTGTACTAAAAAATACAAAGTTTAGCCGGATGTGGTGGCACACACCTGTAGTCC<br />
CAGCTACTAGGGAGGCTAAGGCATGAGAATTTCCTGAGCCTGCGAGGCGGAGGTTGTGGTAAGCCAAGAT<br />
TGTACTCCAGCCTGGGTGATAAAGTGAGACCCTATCTCATAAAAAACAAAAAAACAAAAAAGAAAAAAGG<br />
AGAAGAAAGAGACACAGATTAGCATTTGAATGGGTGGACTGAGTAAAGCAGATGGCCCTCGTCAGTGTTG<br />
GTGGGAATTGTCCTATCCATTGAGGGCTTAAATGAAACAAAGACTGAGGAAGGCTGAATTCAATCTCTGC<br />
TGACTGCTGGGGCTGAGACATCAATCTTCTCCGGCTCTCAGTGCTCTTCCAGACTCAGACTGGAATGTAC<br />
ACTATCAGCTCTCCAGTTCTCAGGCCTTCAAATTACACCTCTGGCTTTCCTGGGTCTCCAGCTTGCAGAT<br />
GGCAGATCGTGGGACTTCATGGGACTTCTCAGACTCCATAACCAAGGCTGAGGAGCTACAGTCTAAATGC<br />
ATACGCATGTTGGGAACCGAAGTCAGCCATCTTCCCTAGGACAAATCTTTACTCTTCTAAAGAAGGACAA<br />
GAATAAGAATTGAAAACACTTTTCACAGTATAGACATCTATAGTGTGTAAAACCATCTTTACAAAACCCA<br />
TATATACAGAAAAATCTCAGTCTTCAATTTGAAGGTTCTTTGCCGTGCTAACATATGTTGTAGAGAATGA<br />
CCACATAGTAATTGTCTAGTCTTTTCTCCTAACCCCAATAGGATTTGAATGACTTTCATCGTAATGAAGG<br />
CTTCTGCAGAGTAATTGATTTTGACCATGAGTACCTGTTGAAGTCACAGCAACTTCTCCTTCTAGATTAT<br />
CTTACAGCAGTGGACCAGACAGCAGTGCTCAAGAGAGAAATGCTATCAAACAAAAAGTGGTTCAATACTG<br />
GCATCCTGTGGCTGGAGAGATTTATCAAATCTCTGAAAATCTCAGCTCCTTGGATTCTGAACATTCCCTG<br />
GCTGTCAGTTCTCAGCAGCCTTTCACCATTTTCCGAGTGCTATTTGGTTACCTCTCATTTTTCATGGAAA<br />
CAACCTAGGTAAAATGCATTTTGATAGACTATCATTTTCACAGGGCTGATCTACTCATGCATTATCAGGG<br />
TAAAAATAAATGATAATATAAAGGTTTTGGAATTTTACCTAATGAAAGAACATGATATTAAATCATTGAA<br />
CAAACTGCTCCAAGCAAAGGCTCTTGGTCTCTAAGTTCACATTGAGTTTCTCTCTAACAAAATGATCATA<br />
GAGTAGTTGGGAGAAGGGACAGGGCGCTGCTTCAGGATTTTGTTGTTTGTGCGTCTGTGTGTGAGTGTTT<br />
TGTTTTGGCCAAAGGCTAAGAAAATACTTCCTATTGCAGCAATAAATATTATGAATTTTCTTTATTTTAC<br />
TACAAGAATGCTGCCTCAGAGAAAAATCAAACAAAATTACGGAGGACTGTTGCTTTTTGCTACTCACTTT<br />
CAAGGCAGCTATAAAGATAAAGAGTTACAATGATCGCAGTTTAAAAGCAGAATTGCCATGCTCCCTGGTA<br />
AGACTTAATGGCATTTTTGAGAACCAAATAACCATTATGGGACTACTCCATTGCTGCTAGTTTCACAAAT<br />
GGCTAACACTAAATTTGGAGGCCTTGGAAATGTTCAAAACATCATTAGAGATAGAAAAATAGCAACAAAC<br />
TTTAAAATTACATGAACACCAAAAGACATCAATGAAGGATCAAGCATGAAAACCGCTTGTTGAGATGAAC<br />
TGACAAAGAAATAATACAAAGTACACACGTGCTTGTTAGCAAGAGGAAAGAACTATTAGAGTTGGCTGAC<br />
TCCAAACAGGAGGAACAAAATGCCTGCTAAAGTGGGATCGAACAATGGCTTTGCTCTTTCATCATGCTCC<br />
CTTTCTTCTAGTCTAACTCTAGGACCACCAGCTCTTTCTTCCTCAATTCTCTTAATTTTCTGTGCTGCTC<br />
AGGGGTTTTAACTGTCTTGGTTAGTATGGGAGACAGACAGATTTCACAGCGATGAGTGCTAATCTATCCT<br />
AAATGTTAGCAATGAATAAAGCAACCCTAATGGTAAATGGTATTTAATAAGATCCCTTTTCCCTCAGAAC<br />
AGGCTCTATATTTAGTGTCTAGAACACAGAAAACTTAAAAATATTCCACAGAAAGCTAGTGTGATCTGAG<br />
AAGAAATAGAGATTAAATACTCAGTTAAGGCAATCAGTGTGCCTGTGTCAGCCATAAAGCACCTCATTTG<br />
TATAGTAACATTTCTTTGGGGAAACAAAATCCAGATATAAATATTAGTATAAGATCTAAAGATGCAAAAT<br />
TCCAATTGAATGCTAATAAAAGGTATTAATAAAACTCTGCTTTAAAGGACTGACTTCTCAATGAGTCTGC<br />
ACAGCACACTAGAGATTCAATATGCATATCAAGGTTTTTGGTTGTTTGTTTTTTTAGTAACACTGGCATT<br />
ATTTATTAATAATTTAACCAGAAATCTCCCCAAACTTTTAACTGGAATTTAAAAAATTAATTATGGTAAA<br />
GTAAGTAAATTAAAACAAAGAAAAAGTATGAAAGCTATGTTCTAAACTCACCACATTCACCAGCGAGAAT<br />
AGATCTGCCCTTCTGGCTATATTTGTTACCTACCTATCTCTCTCTCTCTCTCTGTCTCTCTCTCTCCCTC<br />
TCTCTCTCTGTCTCTCTCTTTCCCTCTCTCTCTCTCTCTCTCCGCCCCCCCCACTTCCACAAGGGATCCA<br />
GTCTAGAAAGAGCATGAACTTAGAAGTCCAGCAGATGTGGGTTCAATTCCTAGTTCTATGGTTTAAAATA<br />
CATACACTCAAAAATAAATTCTCCATTTTCCTGAGCTCTGGTGTTCTCATCTGGACTTGGGAATAATAGC<br />
ACCTCACACATCAACCTTGTTGAGGATTGCTTGAGATGATCATGTAGGGGAGAGGACTCAGGAGAGCCTC<br />
TGACAGAGAGATATGCTTTCAACACAGGCTATTCATAAGCACCCTTCCTACCTAGTCATCTACTATGTTT<br />
TCTCCTCCCCCAGTTTAACTGGTCACCAAGTCTTGCTGATTTTTCCTTTTAGTATGTTTCACTTTCTCTC<br />
AGACCCTGCTGATACTGCCTGTCTTCAGAATCCCCCTCAATTCTCATCAGGATTGCTGCAGTAACCACCA<br />
AAGTCAATATTCTGTCTTCAGCCCCAACCTATCTTAATCCATCCTCATAACCCCCAGGGTGATTCTCCTA<br />
AAATATAAAACTGCCTGAGTTTGACTTTCAGCTATTCTACTTTATATCTGTATGACTTGGAACAAGTGAC<br />
CTGAATTCTCTCATGCTATAATTCAAAGCCTATTAACTGGGGATAATAATTTTCCTACCTCAGTAGGATA<br />
TTATATGAATTAAATAAAGTCTTGTTCCTCTCCCAAAAAAAAAAAAAAAAA</dnaseq><br />
<br />
<br />
==Labs working on this lncRNA==<br />
* The Department of Gastrointestinal Surgery, The Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan, People's Republic of China.<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Luo Y, Wang C, Yong P, Ye P, Liu Z, Fu Z, Lu F, Xiang W, Tan W, Xiao J. Decreased expression of the long non-coding RNA SLC7A11-AS1 predicts poor prognosis and promotes tumor growth in gastric cancer. Oncotarget. 2017 Nov 7;8(68):112530-112549.<br />
</ref>(1)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=MAGI2-AS3&diff=1276488MAGI2-AS32019-08-13T07:55:15Z<p>Qianpeng Li: </p>
<hr />
<div>==Annotated Information==<br />
<br />
===Name===<br />
Approved Symbol: MAGI2-AS3<br />
<br />
Approved Name: MAGI2 antisense RNA 3<br />
<br />
Alias symbols: ENST00000414797<br />
<br />
Chromosome:7q21.11<br />
<br />
RefSeq ID: NR_038343<br />
<br />
LncBook transcript ID: HSALNT0289161<br />
<br />
===Characteristics===<br />
-<br />
===Function===<br />
<br />
* MAGI2-AS3 significantly inhibited breast cancer cell growth by targeting Fas and FasL<ref name="ref1" />.<br />
<br />
===Regulation===<br />
-<br />
===Diseases===<br />
Breast cancer<ref name="ref1" /><br />
<br />
===Expression===<br />
[[File:MAGI2-AS3-1.png|right|thumb|400px|lncRNA MAGI2-AS3, Fas, and FasL expression levels in breast cancer tissues and breast cancer cell lines.<ref name="ref1" />.]]<br />
MAGI2-AS3 is down-regulated in breast cancer tissues compared to normal adjacent tissues<ref name="ref1" />.<br />
<br />
{| class='wikitable' style="text-align:center"<br />
|-<br />
! | Experiment<br />
! | Forward primer<br />
! | Reverse primer<br />
|-<br />
| rowspan="1"|Quantitative real-time PCR<br />
| | 5'-CACCTTGCTTGACAACTTGA- 3'<br />
| | 5'-CATTACAGCTCGGCTACTGC- 3'<ref name="ref1" /><br />
|}<br />
<br />
===Evolution===<br />
-<br />
===pubmed IDs===<br />
27816668, 29679339<br />
<br />
===Sequence===<br />
>NR_038343.2 Homo sapiens MAGI2 antisense RNA 3 (MAGI2-AS3), transcript variant 1, long non-coding RNA<br />
<dnaseq>GAGGCAGGCTGGGTCCGCCTGGCAGCCTACGGGAGGAGGCGGGAGCCGGGAAGGAGGGGAGCCTAGGCCC<br />
GGCGTGGGGAGGCCGGCAGGAAGGGCCTCGAGCCCAGTGCGGACCTTTCTTCAGCCTCTGTGCGACCGAG<br />
CCGCGCGCCAGGCTCCTGTGCGAGGAGGACGCGCTGACTCCCTCCGACCTGGGCTCCGATGGAGCAGAAA<br />
TAGCGGGACCTGGACTTGTGGCGCGCCTGGTGCCACATCTCGGGCTCTGCGAGCGTCCTGGCGCGGGATC<br />
CTGCCGTTTGCATCCAAGAGAGGGGAGGACAGGGGCAAAAGGATGCAGGGAGGCTGCTGATTTCCACTGA<br />
AGAGCTAATTTCCTGTGAGACATTAACAGTGATTTAAGAAAAAGATTCCTGTAACTGTAATGTCTTACAA<br />
TAACAGAATGCAGGAGAGCACATATCAATGAAGAAAAGACAAAATGTACTTATCCATGAAGCTGAGGTTA<br />
AGAAACCAGTGTCTTCAAGAGCCAGGGACAGCACTGGGTCTGTGCAGAGTTGAGAGATGGTGATGACATG<br />
TGGTTTCCAGCATTCCTCACCCAGTCCAGGGACACTGTGGGTGTGCCCAGCTTAAGTCCAGTAACTGGAA<br />
ATACAAGCCCAAGTTCTGGAGAGTTTGAGCTGCAGAGATATATATGGGAACACTTTGAATCTTGACTCAT<br />
TGGCCATAACCAGCAGAGTGGAAAATACAAGAAGAGAAAAAAACATTGAACTGCGATTTTATAACATCCT<br />
TTACTAGGCAGAGAGAAGAGGAAACACCAGGAAAGAAAACTGTATTACGATGTGAAAACTTAATGTTGAG<br />
AAATTCAGGCATCTTGGGGTTAGTGAGGAGAAGTTTTAGGGGCTTAGATTCTTCTAAACACATGTACAGA<br />
AATGCATATTTCATCTGATATCAAATGGCATTTATAGTGCTAATCTTTACCTCAAGACTTCACATCTTTT<br />
GGTGATTGCATCTTTTAGGTTTATAGCAGCTAAGTTTGCATGAAAACACCAGGGCTGTTTCATTTCAGTC<br />
AAGAATTAATGTTCATTGATTGTGCTTCTGCATTTCATGTAACTATTGTAGAATTTGTTTTAGTTTTATG<br />
AGGGAATAATTGTTCCAACTTCTATATAACTCAGGAATTTACTCTCAAACAACACTGTCAATTAGTTACT<br />
TATCTCTCTGGAAATGATCTGGGAACATGGAGAGGAAAGGGAGGAAGGGGCAAAATCTGACCACTTAAAT<br />
CTAAGCATATTAGATCATTTTATGCTAGAAAGTCCTGAATGATGTGACTTTCGTTCTTGTAAAACACCTC<br />
TTTCCATAGATTCATGGCCCAAACAGTATATAAAGAGTGGGGAAGGAACTGCATTTGCAAATAGTTCAAA<br />
TCATTGCTCCATCTTAACTACGCAGTTCACAAAGTGTGAAGAAATGTGATCATCTCAAAAAAGATAATGG<br />
GGAAAAAATATGTTTTGTTCTGTGACTTTAAAGTCTTGCAATATTTTACATAAATGATAATGGGTGCTTT<br />
AATAAGAACTCTTGATACTTTTGTTATTGTATTCAATATATGCATATAATACAACAGGATGATATTGTTT<br />
TGGATTTGGAAATGTATTCTTTCTTATGCAATCTTATGCAGTCATACTGCTTGAATATCATTACCTGAAT<br />
TTATCTTTCTTTTTTTTGTTGTTGTTTTACACTCTACTTATTTGGTGCCTGTCAGTCTTTTGTCGTCAGT<br />
TTATATTCTACTAAACTCAAAAAGACAATCTCATACCTTTTGTAATTGTAGGCATTCTTTACTAGATTTT<br />
TAAATACACTTCAAAAATTCAAGTACTTTGATTTCATGCCATCAAGTAGCTGAATCTATCCCCCCGTCTC<br />
TTTTTAAATTTAAGTGAGTAGTTCAATTTCTGTCACTTTCTACTTTGTGAATTCTAAATCTTTTAAAACC<br />
ATCTTGCCATTTTTCGTGCACTTACCCTTACAGAAAACTCTGTGAAACACTACTTATCTCTACTTTTATG<br />
TTTTTAACTCCTTTTTTATATTACTATTCCCTCTGCTTTCTAAATGCACATATTAATTTGTTCTTTTTAT<br />
TCTCTGTAGCTCTTCTCAGTGTATGAATTCAGTTTCCCATCAGTCTCCATACAATTAAAAAAAAGTTGAG<br />
TATTCTGTTATTTTAATAAGATATCTAGTGCCCATATTCTAATTCTGCCCCTTATTTTTAATATAATTTT<br />
ATTGTTGATTTAAAATGACAACAGTTTCAATTCCCAGAAAGTGAAAGGAAACAAAGGAATAATATTATAG<br />
GCTTAATTTTTATCAGTGAACTTGTAGGTGAAGAAAAGATTTGGGGAAGGAAATGAACATATTATATTGC<br />
AAAATAGTAAGGAACAATCAGATGTGTTTTCTAGTCTCTGGAAAAGCATGTTTCAAGAAATTCAATGAAA<br />
AGTTCATCATGCTTGCTTAGATTGTTGAGAAGCAAAAACACTGATGAACATTTGGAAGCAATGAGAATGT<br />
AATTCTAATCATACTCTTTTAATAATGTTGCAAAACTCTCCAAACACTACTCTGTGTGGATGTCTTTCAG<br />
AATATGATGAATACTAGTAGTCTTATTCTGCCCTTTTCTCTCTATCACAATATATACATTCTATATTGCA<br />
TACACATATTTTCCAAATATTACATATAATTTCATGTAATTTATAGACCTATTAAGGCCCAACCATTTTC<br />
TTGGATAGGGGATTCTTTAGAAGTCCAGCTTAAATAAAGCCCGTATAGAAAGTTTTTTTAAAATTTATAC<br />
ATAATCACCTAAAGTAACCTTATCTACTGAACTCTTAGTACATGCTACTGGAACCTTTTATCATGTTTCT<br />
TCCTGGCTTGCATTACAACACTGTTGACATATCTCAGCCTTACTTCTAGGCTTCTTTGAGAGCATGACTC<br />
ATGTTTGTATTCCTCACTGAGGTTGAATGAATAAGAGAAACTACAGTAGTAGGAAAAAACAGTACATGTA<br />
CATATCAATGAATATGAAAGGGTCAAATGGATCTATTATAGTAAGCACAAAATCAACTGACACCAGCAAA<br />
GTAAACCCAAAATTTTTAATGGTATTTTAATAGATCAAGAGGAGCAAGCAGATTTTTGAGACAGTTGTCT<br />
CCTACTTTCTCTATCACAGGGAGTAATTTTAAAAGAAAAATGGAGGGTAAGTTTCTTTAAGAGAAAATTG<br />
TAGTTTAAAACAGGTCATGGGATAATTAGAAATAATTTAATTTCTTTAGAGGATTTTAATCTTTCAACTG<br />
CTTGCAATTAGATCCTAAGGCAATAAAAGAATAAGGAGATTTGGAAAACCATTGTCTGTAATCTCTGAAG<br />
AAAAGTGGACATTAGGGGAGTCAGTTGAAAAGCAAAGCTATCACCATTTTCTAAAGAGGAAAAAGGTGAA<br />
CCTCACAAACTATAGACCAAAAAAATAGGACATCGAGAGAAAGAATATGAAGCTAGCATAGGTTCACAAA<br />
GAATGAGTCAAATCAAACAACATGCATTTTTTATTTATAAAGCATGACTTGTTCATTGTCAATTCATGTT<br />
AGCTTAATCATTAGGCATTAATGCCATCACTGCAATGCATATGTCAGCAATAAATAATCAAAGACCAGGC<br />
TTCCATCATTCTGTTTAATATCTTCAAGTAATGCTTAAGTTTGCAAATGCTCTTTTAACACATTCTCCAT<br />
ATGCAGCCTGCCCAGCACTGCACACAATAGACCTGTTACTTCCCCCTCACGAGCACTCCTAATATTTCAT<br />
GTGCTCATCCAATTGACTTCTCCCACTGGTGCCTCATATTGAATTTGTAGAATCACACCTGCTCCTTTTT<br />
CAAAACTCTTCTGAGTTTTTTCTTAAATAATTCACTGACCCCAAAGTTGTCAGATATTTGAAGACTACTC<br />
GCACAATTTTAATATTATAAATGTATAATGTAAATGTAATTAAGATTTGTATAATGTACGATGTACTTTG<br />
GTAAATAAAAGTATGCTGTGAATAAATACGTATGATACAATTCAAAATTTTACATAAATATGTGATAAAA<br />
TTTAGCTCATATTCTTTTTTTTTTTCTTTGAGACGGAGTCTCACTCTGTTGCACCCAGGCTAGAGTGCAG<br />
CAGCATGATCTCAGCTCACTGCAACCTCTACCTCCTGGGTTCAAACAATTCTCCTGCCTCAGCCTCCTGA<br />
GTAGCTGGGATTACAGGTGCCCGCCACCATGCCCAGCTAATTTTTTTCTATTTTTGTTGTTGTTGTTGTT<br />
TTTAGTAGAGACGGGGTTTCACCATGTTGGTCAGGCTGGTCTTGAACTCCTGACCTCAGATAATCCACCT<br />
GCCTCGGCCTCCCAAAGTTCTGGGATTACAGACGTGAACCACGGTGCCCGGCCTAGTTCATGTTCTTTAA<br />
GGACAATTATGAATATTTTTATGCACTGTTAATTTTCATTAAGATATTGATCAATTAATAGCTATATATG<br />
TTCTATAAATTAATCCTATCTAGTTTCAATCTTAAATTGTTTGCATATACCAATCTAGTTTATTGTTTGC<br />
ATATATTTTATAGTGTAGAGATTAGGCATTTTAATAAAATTTTAAAATTTCCAGGACATACTGTTAATGA<br />
CTATGCTTCCTACTATAGGCCATAATTAATTTTTTTCTATTGTCAACAATATTTTGGTAGGGATGATCAG<br />
GAAATAAGGAAATGTTTCCTTCATTTGTTAACAATAGGTGTTTGGGGATTTTAAAATGAAAATTGAAGAA<br />
GTAAAAGACACCATATATTTAGTTTGTTTGATTTCGTGGCTTCAAGAGTTCAATAATTTATTGAAATATT<br />
TTACAGACCAAAGAACAACAGATATATTACGTTTATAAGCCCCCACATATTTTAAAGGATAATGGTTTAT<br />
ATATGAAAATTCCCTGAACCTACACTTCATCAGGAAAAGCTAAATAAAAGAAGTTTACATTTCCTAGGAC<br />
TAATGGAGATTTATTTCCCAGTCCTCTTCTCTGGAGACAAATGTAGGTCTCTCTTGAAAAGCAGAAAGTT<br />
TTGCATATGAGGTATGATTTAGTGGGCTAGAAACATCTTTTCCACCCTCCCCAAAATGTTTCACTATGTT<br />
TTATCATACTATCTGATAATTTTGCACTAAAGTTTTCTTTCTGTGTTAAGAAAATGCAAATATCTCTGAA<br />
TGGGTCTCTTTGCTTTAGTCATACTCATATGGCTACTACTGAACAAAATATGTTCATTACAGGATGAAGG<br />
GAATGTTGCCAGCCAGCAAATCCCTAGAGTTTGCACTACACCAAACGTTGCTTAGCAATTTCCACGATTT<br />
TCTCAGTCTAATTTGCAAGAATCAAGGAGATGTTTGTGTATGCTACATGAAGTTGTAAAATTGGTATTTA<br />
TTGTATGTTTCTATATCGAAAGCTTTACAAACAAAGGAAATGGAAAGTTAACAGGTGGATATGATAGTGT<br />
GGCACTACTTTAGCTGGATGGTAAGGGAGAGCTTCTCTTAGGAAGTGTTTTAGGCCAGGACTTGAATAAT<br />
GAACAGTATCTAGTTGTACAAAAATCTGGAGGAAAGACTTTTCAGGCCCAGGAGAAATGAAAATTCTTTT<br />
CATGCATACAAGAATGAAAGTGAAAATTACCTACTCTATGTCCTGAAGTGGGAAGTTGGCTTGCCAGAGA<br />
GTAGGTAATTTTCACTTTGATTCTTTCATGCCTTCAGTTATACTACTTCTTAGGTTAGTTCATAAGGGTT<br />
TCCACAATTTGGTTCCCACTTAAAATTTAAAACTTCCCTAACCCATTCCCACCATATATTGTGCTAATCC<br />
ATGCATATGTGACTTTGCGTATGCTGTTTTCATTGTTTAATATTCTTCTCATGCATTCGTTCTTTCCTGA<br />
TAACGAACTCATCTTTGAAACTCCCCTTCAAGCATCCTCTACTTTAGGAGGCCGCTTCTCACTGTCTCCT<br />
GCCTACCACCCATTGAATTGTTCAATTTTTAAGCTGCCATTGTCTTGTGCAGTTGACACATTTCTTTGCA<br />
ATTACTGATTTACATGTCTGCTTTTATCACTGGTGAGGTTCTTTAGGACAGAGACATTATTAATTCATCT<br />
CTGGGCACATATGTTCCAACATATTAGAAGTACTACAGAGTGCTATTACTATGTAGTATGTAGTATTAGT<br />
AGTAGTTACTCACAAATCATTTTTAAATAAGTGATTATAATATCTTTTTGTTATTATGATTTAACACAAG<br />
ATGGAATTTATTTTCAGAAGTTTCCATGATATATTTGTTCTATTTAAAATCCAATAGCCATTAGAATATT<br />
ACCATTATTTAATGTAAAACAATAAAATATTAAATATGATCGTTCATATTTAATGCAAACCGAACTCATG<br />
GAAATATTGTGTAAAGATCAAGTAATTTTTGACATACAATTTTAAACTCAACTTTTCATATAGCATACCT<br />
TATGATATATTTTCAGCCTACTTTTAAATATGTTGGCATTGAAAGCCAGTTACTAATTCGCTGAATTCAT<br />
GATTTCTTTTTAAGTTATAGAAGTGGAATTATGTTTGAGATATTCATTGCATTACATTTACCAGAACTTG<br />
AGTTCTTAACATGGAACCTGAGAGTTTCTCCAATTCTTAAGTCCCTGGGAGAAATAGATTAGCTGGATGA<br />
GGAACTGAGAGGAAAAATGGTCAGAGATGTAGCAAGAGTTGGGAAGAAGGAACAATGATTTGCTTTCAAG<br />
GAGATTTTTTCATTGGTCTGTTTTCAGTGACAAACCCACTGCGATAATACATGTAAAGTGAAAACATTCA<br />
GGAAGTTCCCTTAGAAACCTCTTTTCTGGCAGTTCCTAATTCTACAACATTGTATAAGTGAAATACCATA<br />
GTTACTGTCATAGTAAATTGAGCCAAGAGAAACAAGGGAGCAGGAGAAGAAAAGAATTAAAGAGAGTTTT<br />
GTCTTTCAGTCTTCACTCTGTTTCTTCTTGCTTTTACCAGTCATTCAGGTTTATATAATTTCTTTAGAGA<br />
GGCTTCTACTATGCAGGTCTTCCTTAAAGTCATTGGTATTACCTGGCATGATATGTGAGCCTTTAATATC<br />
AGTCCCTTTATCTCTTTATTTTTAAAGTTTATATCAGTACAGAGTCCTGGATTCTTAATTAATTTAATAG<br />
GTTAGACTTTATGCTAATATTCTTCATTTTGATGCTCAAATTTTCCAAAATTTGGCCAGCAGGGTTCCTT<br />
AAAGCTGGGTACCTTGCCCTTTCAACATGTCCCTCTGATTCTTTATTTTTATTTACTTATTTATTTATTT<br />
ATTTATTTATTTATTTATTTATTTATTTAGAGACTGAGTCTTGCTCTGTCTCCCAGCCTGGAGTGCAATG<br />
GCACAATCTTGGCTCACTGCAACCTCTATCTCCCAGGTTCAAGCAATTCTCCTCCCTCAGCCTCCCGAGC<br />
AACTGGGACTACAGGCATGTGCAACCATGCCTGGCTAATTTTTTTTGTATTTTTAGTAGAGACAGGCTTT<br />
CACCATGTTGGTCAGGCTGGCCTCGATCTCCTGACCTCAAATGATCCATCGCCTCGGCCTCCCAAAGTGC<br />
TGGGATTACAGGCGTGAGCTGCCACACCCAGCCGTCCCTCTCATTCTTTAAGTACTTCCATGTTTTCTAA<br />
GGTACAAGATGTTCCATATTATTTTGTTATTTGTCTTCCCCAGCTCTGAAATCTGCCTTTCCTTCAAGGA<br />
GCCTTGGTTCTTTCTAGTGACAAATTATATTTAGAAAGAAGATCTGGGTATTTGACTTGTATATTGCTAT<br />
TAATTGGCCATTGTTTCTAGTCTCTTTCAGTAGACAGAGCTAAGAAATGTAAAAGGAAATATTTGAATGT<br />
ATGTATATGTGATATATTAAGTACATTTAAACATATTAAATTCATGAGTTCATACTAATACTTTCAATAA<br />
GCCACAATTCCCTTTTCATGTTTTCGAAGGAAAAATATCCATTGTCTATATACAGTGGACATAGATAGTA<br />
ATAATACTGATCTTGAAAAGAGCAGTCTTAAATAGATCCCATTAATAGTTAAAGATAACATATCTTAGAA<br />
TTCTAGATATTAGAGAGATTATCTAGAGCTGTAATCTAGATATTTTATAGATCTTTGCTGTGCTGTTTTG<br />
AATTTGTGTTGGAGTAGAACAATCAGATGACAAAAGCTCATCCCACATGGAAAAATCAAAGCATTCATTA<br />
CAGAGAGAATTTTGAAATAAATGCATATATAAAAAATATATATGCATATATAATGCATATGTATATGCAT<br />
ATAAAATATATATATATAAAATGAGGGTTATAAACAATGAAGGAAATAGTGATACTATCTATGTGGGAAC<br />
AATACTAGTATCCTCCCTTTGGATGAATACAGTAGCTACAGATGCAATTCTGGGGACTCTGTTTAGCAAT<br />
AGCTTAACTATTGCTTGGCTACAAGCATGGATAACTTGTTCAAAGATAATGAGGAGTTGTAAATATTTAA<br />
ATAAACAGGATTTGCAACATAAAAAAAA</dnaseq><br />
<br />
==Labs working on this lncRNA==<br />
* Affiliated Hospital of Taishan Medical University, Tai’an 271000, Shandong, People’s Republic of China<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Yang Y, Yang H, Xu M, Zhang H, Sun M, Mu P, Dong T, Du S, Liu K. Long non-coding RNA (lncRNA) MAGI2-AS3 inhibits breast cancer cell growth by targeting the Fas/FasL signalling pathway. Hum Cell. 2018 Jul;31(3):232-241. <br />
</ref>(1)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=EPB41L4A-AS1&diff=1276487EPB41L4A-AS12019-08-13T07:39:48Z<p>Qianpeng Li: </p>
<hr />
<div>==Annotated Information==<br />
===Name===<br />
Approved Symbol: EPB41L4A-AS1<br />
<br />
Approved Name: EPB41L4A antisense RNA 1<br />
<br />
Previous Symbols: C5orf26, NCRNA00219<br />
<br />
Synonyms: TIGA1<br />
<br />
Chromosome: 5q22.2<br />
<br />
RefSeq ID: NR_015370<br />
<br />
Ensembl ID: ENSG00000224032<br />
<br />
LncBook transcript ID: HSALNT0288958<br />
<br />
Pubmed IDs: 9490301, 30796006<br />
<br />
===Characteristics===<br />
-<br />
===Function===<br />
<br />
* EPB41L4A-AS1 could alter glycolysis and glutaminolysis levels of cancer cells. Furthermore, EPB41L4A-AS1 knockdown plus glutaminase inhibitor suppressed tumor progression both in vitro and in vivo. Mechanistically, EPB41L4AAS1 interacted and colocalized with HDAC2 and NPM1 in the nucleolus, controlling HDAC2 occupation and H3k27ac modification levels on VHL and VDAC1 promoter regions and regulating their expression, which affected glycolysis and glutaminolysis<ref name="ref1" />.<br />
<br />
===Regulation===<br />
EPB41L4A-AS1 expression was transcriptionally regulated by p53 and PGC-1α<ref name="ref1" />.<br />
===Diseases===<br />
Human cancers<ref name="ref1" />. <br />
<br />
===Expression===<br />
[[File:EPB41L4A-AS1-exp.png|right|thumb|400px|EPB41L4A-AS1 expression was downregulated in human cancers<ref name="ref1" />.]]<br />
EPB41L4A-AS1 is down-regulated in some human cancers. The low expression of EPB41L4AAS1 was associated with poor survival in several cancer types, including<br />
cervix, liver, breast, bladder and other cancers<ref name="ref1" />.<br />
<br />
<br />
===Evolution===<br />
<br />
===Sequence===<br />
>gi|284005302|ref|NR_015370.2| Homo sapiens EPB41L4A antisense RNA 1 (EPB41L4A-AS1), long non-coding RNA<br />
<dnaseq>TGTCGGGTCCCAAAATACGTGGTCTAAAGTCCTTTGGGCTCCTGCCGCTGCCAGCACTGATCATATGCTCTTGACCCTGGTCGGGTGGGGGGATGTCTGGATACCTCCTCTGTGGAAAGAACTGGCCACACATCCGCAGAGGTGACTCGGGCTGAGAACCCAGGCTCCTCCTCCCTTTGGTGACACGCCCCTCGGTCCCTCACTGGCACTTCTCCCTCCGGCCACACGGCGGCGTCTCGCCATAGCGCAGCGGCCGATGGTACAGCCCGCTCCCCCCTCGCGCTCTCGGACAGTGGGTCCTTCCACTTGTAGAAAAGCATTGTGGGACGGAAGCCTGTCCTTTCTTCCTTTTGGTGCGAGCTTGCTGTGGTTTTTGCTCTGGGTCCTCTGGGATGGCGCCTGGCTGTGGCCGCGTGGTCTCTCACGCAGGGGCGCCGGGCGGGGGAACGCGGCCACCCTGAGTCTGGTGAGTCGACTGCGGCGGCCTGTGTCCGAAGTGTCCGGGGCCGTGAACAAGGGCAGCGGCCTGGCCTCAGGCCTGCGTTCCCACGTTTGGAAACGGGGAGCTTCGTCGATTTGTGTTTACATCATCGACTATGCCAGGGAGTTCTCCAGATAAGCCTGGTTTTATTTTCGTCAGTGAAAAGGCCTTACCGTATAACTGACTTTATGCTTGCCCTGCCCCCGTATAAAATAACTTAAAAGCAGCGTGCCTGGTTACAGCTGTTTCCACGTGCGGTGCTCGTCGGGAGTGATCACCTACCCTACAGGTGGAAGATGGATGCCTGAAGTGTAGACTGCTGCTAGCTGAATACCATCTGGGAGCATAAAGGTGACCTGAAGGATGTCCTTGGTGAGGATTTTGAAAATTTGATCTTCACAAGAGTTGCCTGGATCATTTGAAATTTCTGGGAGTCTGAGGAGTACTGACATAATTACCTGCTGGAGTCTGTAAATACACATTTAAGACAGTGAGGATGTGAATAAATATATTAATGCACTTTGGCATTTGTGTTTTAAGTGATTAACTGCCAGAAACAGCTATTTCTAAAAAGTTATAAGGGAGGAGGGGTTCTTTTTTGATCAGTATTCACTGCTGTCACCATAATTAATAGCCTTAAAATAGCTTGTGTTTGGCCCAAAGAGAAATGTACTTTCTTCCAGTGACTCAAAAATCGTGGCTAGAACTAGACT</dnaseq><br />
<br />
==Labs working on this lncRNA==<br />
* School of Life Sciences, Tsinghua University, Beijing 100084, PR China<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Liao M, Liao W, Xu N, et al. LncRNA EPB41L4A-AS1 regulates glycolysis and glutaminolysis by mediating nucleolar translocation of HDAC2[J]. EBioMedicine, 2019, 41: 200-213.<br />
</ref>(1)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=DDX11-AS1&diff=1276486DDX11-AS12019-08-13T07:38:52Z<p>Qianpeng Li: </p>
<hr />
<div>==Annotated Information==<br />
===Approved Symbol===<br />
DDX11-AS1 (DDX11 antisense RNA 1)<br />
===Synonyms===<br />
CONCR, SCAT4<br />
[[File:CONCR Is a Nuclear lncRNA Negatively Regulated by p53 and Activated by MYC.jpg|right|thumb|400px|'''DDX11-AS1 is a nuclear lncRNA negatively regulated by p53 and activated by MYC'''<ref name="ref1" />]]<br />
[[File:CONCR Is Upregulated in Multiple Cancer Types.jpg|right|thumb|400px|'''DDX11-AS1 is upregulated in multiple cancer types'''<ref name="ref1" />]]<br />
===Chromosome===<br />
12p11.21<br />
===RefSeq(supplied by NCBI)===<br />
NR_038927<br />
===LncBook transcript ID===<br />
HSALNT0288928<br />
===Characteristics===<br />
DDX11-AS1 is a divergent non-overlapping transcript of the protein-coding gene DDX11, which is a predominant nuclear lncRNA. ChIP-seq data from ENCODE shows that MYC is bound to DDX11-AS1 promoter region in multiple cell types.<br />
===Expression===<br />
DDX11-AS1 is expressed in a panel of different human cell lines and upregulated in multiple cancer types. <ref name="ref1" /><br />
<br />
The temporal expression of SCAT4, SCAT5, SCAT7, and SCAT8 elevated during S-phase in serum-starved Caki-2 cells<ref name="ref2" />. <br />
<br />
===Regulation===<br />
DDX11-AS1 is negatively regulated by p53 and activated by MYC. <ref name="ref1" /><br />
<br />
===Sequence===<br />
>NR_038927.2 Homo sapiens DDX11 antisense RNA 1 (DDX11-AS1), long non-coding RNA<br />
<dnaseq>GCATGCGCACTCCGGGACGCGCGCGAACACGCAGCAGCGAGAATCTACAGGGGCGTGGTTTGCGCACGCG<br />
GGAACTGGGATCTCAACCCCAGGGCTAGGTGCCTCCTCCCGCTGCTTTCCGCCAGCTGCGGGGTGTGAGA<br />
TTAATCCCCGCCGATTAGCGCCAGGTGTACTAAGCGCTGGATGGTTCCCTGACCAGATGAAACATCAGCC<br />
GATGTTCTAATGCCGGTCCCCTGGGCGCTGTCCCCGAGAGGGAAAACCTGTTTTCTGACCCCGGCTCTAG<br />
TCGGCCTCTGGAGGTCTGCAGCTGGGTTATTTTACCTTTGAAACGGACGACACCTGCCCCGTGCACCCCA<br />
GCGGCTCCTCCACACGGAGAGATGGTGTCAGTCAAAGGCCGTCTAGATGACGAGTTTATGAAATTGTTCC<br />
TGGCCCGTGCCGGGCACGACCTTGCAGAGAGCCCAGAAGATGAAACCCCAGCCCTGCCAGGAGCTCACCT<br />
GCTAATTAGGAGGACAACGAATCACCTCACCTCCCTAGACTTTGCTTCTCCTTTATTCAGTGAGGGATTG<br />
GACTAGCTGGTCCTTGAGGACTTTTCAGAAAGTCTGGTTCTGGGAGATGACCAATGGGATCATCTTATGC<br />
TATGAGCTTTCCTGGAATGACAGGTAATGGAGAGTGAGGAGATTTTACCTGATATGGTCCTGTTTGCACC<br />
ATCAGCCAGCAACCTTTCTGGGAAGCGTGCTTATTATGTACCAACATAAAAGCTTGAATATAAGGAATCT<br />
CACATCTTCTGCCAGCATCCTGAAACTATGGCAGACTCACTTGTTAACTTTGCAAATAAGGTCAAATTTC<br />
AGAACCTTCACAGCTCCTGATAGTCACCGTGTAATAGAAGATTAAAAGACAAGCTCAGCTCTTGTTCCAG<br />
TCAGCCTCATTCCTCTGCCTACAATACAAAAGTCACTCAATCATATTCTTGTCTTAAATTGAACAGTCCT<br />
TACATGGTTAAGAAAAGGAGAAATTCATTGTAAGGAATGTTTACATTTTGTTTATAATTCCTGCAAGTGT<br />
AATGTTTCAAAAGGTTTTCCTGTGGCTGAAGTACATTTACCCTGTGTAGCTCTAGAGAAATGAACTTACA<br />
AACTGAAAAATTTCAGCTCAGTATATAAAGAAAAACAGATTTTCACAATTAGATCTATCCCAAAGAGAAT<br />
AAATTTTGAGGTGATAAGCTCACTGCTGGCTTAGATCATCACTTATGGGACCTCTAATGGGGCAGGGATC<br />
AGACTAGATGTGTACAAAGATCTCTTCCAACTGAAGCTGCTACTGTGGAGGACGTTGTTTTCAGTGGACT<br />
CTCTAATCAGATTTATTTTCATACCAAGAAATGAAGAAGGTGAGCTGGGGGATGCAGCTGGGACTCAGAA<br />
GACTGCACGTGATAGACTCATGAGCTGAAGATCTCGTGCTTAGTCTGGAGAAGCTCATCAAGTCTAGCTC<br />
ACTTTGGAGTAAGTTGGTGCTGGAGAATGAATTCATGCTAACCAAATTCACCAAGAGCCTGATTTACAAA<br />
TGAGAGAGCCAAGGCCTTAAGTTTAGAGCAAAAGACAAACTTCCAATGACTTTAGTTTTCTTGTCCAATA<br />
TCTAGGGCACCTTCCCCTCTCCACCTGCTGTGTACACAGGAGAAATAATCACTCCACACCCGACTGAACA<br />
TTTTCTAACCTTATCACTGTGGCAGAAACTGGCTACTCTTCCTCCTGGGTAGACAGCCAGGCTGTATTTC<br />
CCCGCTGCCCCTGCAGTGAGAGGTAGCCATTGGAGCCGGCGCAGGCCAATGGACTCTGCACTGGAGTGAC<br />
ACATGCTGCTTCCAGGCCTGTCCCTCAAACCTCCCACATGTCCTCTGTCTGCTCTTCTCACTTCCAAGGA<br />
GTGTGACCATCGTGGAAGCCCCAGGTTAGCAATGGCAGATTGGGAGGCATCGATGGGAGGAACCTGGGTC<br />
CCTGACTTAAAGCATCATGGATTTGGACTTTCCGTTATTGAGAAATAAACTTCCATTGTGTTTAAGCCTT<br />
T</dnaseq><br />
===Function===<br />
DDX11-AS1 contributes to tumor growth. <ref name="ref1" /><br />
Expression of DDX11-AS1 is periodic in the cell cycle and its presence is required for efficient G1/S transition and DNA replication.<ref name="ref1" /><br />
Depletion of DDX11-AS1 causes sister chromatid cohesion defects<br />
DDX11-AS1 interacts with DDX11 and regulates its function through enhancing the ATPase activity of DDX11.<ref name="ref1" /><br />
<br />
Depletion of the selected SCATs including SCAT4 in Caki-2 cells altered cell proliferation, inhibited cell cycle progression, and induced apoptosis <ref name="ref2" />.<br />
==Labs working on this lncRNA==<br />
* Center for Applied Medical Research (CIMA), Department of Gene Therapy and Regulation of Gene Expression, University of Navarra, 55 Pio XII Avenue, 31008 Pamplona, Spain; Institute of Health Research of Navarra (IdiSNA), 31008 Pamplona, Spain. <ref name="ref1" /><br />
*Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, NIH Biomedical Research Center, 251 Bayview Boulevard, Baltimore, MD 21224, USA. <ref name="ref1" /><br />
*Center for Applied Medical Research (CIMA), Department of Gene Therapy and Regulation of Gene Expression, University of Navarra, 55 Pio XII Avenue, 31008 Pamplona, Spain; Institute of Health Research of Navarra (IdiSNA), 31008 Pamplona, Spain. <ref name="ref1" /><br />
<br />
==References==<br />
<references><br />
<ref name="ref1"> Marchese, F.P., et al., A Long Noncoding RNA Regulates Sister Chromatid Cohesion. Mol Cell, 2016. 63(3): p. 397-407.<br />
</ref>(1)<br />
<ref name="ref2"><br />
Ali MM, Akhade VS, Kosalai ST, Subhash S, Statello L, Meryet-Figuiere M, Abrahamsson J, Mondal T, Kanduri C. PAN-cancer analysis of S-phase enriched lncRNAs identifies oncogenic drivers and biomarkers. Nat Commun. 2018 Feb 28;9(1):883.<br />
</ref>(2)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=ATP2C2-AS1&diff=1276485ATP2C2-AS12019-08-13T07:33:49Z<p>Qianpeng Li: </p>
<hr />
<div><br />
==Annotated Information==<br />
===Name===<br />
Approved symbol: ATP2C2-AS1:ATP2C2 antisense RNA 1<br />
<br />
Alias symbols : RP11-517C16.2-001 <ref name="ref1" />, RP11-517C16.2<br />
<br />
HGNC ID : HGNC:53167<br />
<br />
LncBook transcript ID: HSALNT0289472<br />
<br />
===Characteristics===<br />
-<br />
===Function===<br />
RP11-517C16.2 shares identical sequences with LoNA on NCL and FBL-binding sites, indicating that RP11-517C16.2 maybe functionally similar to LoNA<ref name="ref1" />.<br />
<br />
===Regulation===<br />
-<br />
===Diseases===<br />
-<br />
===Expression===<br />
RP11-517C16.2-001 is significantly upregulated (33.479-fold) in Botulinum Toxin Type A (BoNTA )(5 U 48 h) treated human dermal fibroblasts <ref name="ref2" />.<br />
<br />
According to GTEx Portal(v7), RP11-517C16.2 is ubiquitously expressed in human tissues, with relatively high levels in brain tissue. We further examined its<br />
expression level in different human cell lines, and found that it is abundantly expressed in SH-SY5Y cells, and barely expressed in 293T, U2OS, and U87 cells<ref name="ref1" />.<br />
===Sequence===<br />
>NR_146503.1 Homo sapiens ATP2C2 antisense RNA 1 (ATP2C2-AS1), long non-coding RNA<br />
<dnaseq>ATCAGAAGGCCTGGGCAGACTTGGCCAGCCACCTGGAGCACTGTGCCCTTAAACTCAGGGCATTCACTGG<br />
TGACCCACACTGACACTGCTTTTTGGAGGACAAGGCAGAGTTGACCATCCCAGTCTTGCCTGGAGGTCAT<br />
AGGACCGTTGTCACTGCAGCCTCAGGTCTGATGCATAATCCCATGACCCTCCAGATCTGAGCCATGACCC<br />
ACTCTGGGCCCTGCCGGCGGGGAGGCGGTGGGCCCATGGGGGCTGCCTCACTGGCCTCCCTCGTCCTCTA<br />
TTCCGGGTTGGGGTTGGCTCTCAGCACACTGGGGAAAAGGGTGGGGTCGATGACTTGTCCCTGGCTCCCT<br />
CCCCTTGCCCCATGCCTGCCATAACCGCAGCTTCAGAGAAAGGTGCCACACTCGCTTGGCTGACAATGTC<br />
GGGGAGTCCCCTGGGCTCCACACCAGGGCGTGTGCCCTTGGAAAACCACGGTGACTGAATCATGTCCCTT<br />
TCAGCCAAAACTGGAAGACAGCCCAGCTCCCTGCCTTCAGGTGACCAGATCTCTAAGTCACATTACTGGC<br />
CCCAGGGTCAAGTCCAGGCTCCCCAGCTGGGGTACCTCCCAGGCTGAGTACAGGCCTTGCTCCCTCCTTC<br />
CTCCCTGCACGTGCTCTGAGCCTCCAGCCCGACGCCTGGGATGCCGGTGCCCCTTGGGCCCCAGACCCTA<br />
CTACTCTTGAGTGACAGGCCTCTTCCTAGGGGTTTCTGTGCATCCGTCACATCACCCACGTTAGAGTCCC<br />
TTCCTGTGAGGACAGAAGGGCCCTGAAGACAGAGCCGGCCCCTGGTGAGCTCTGCTTTCCCGCACTGACC<br />
CCTCCTGGGCTGCAGCTCCCCACCTGGCAGCTGCCGCCCCCCATGGCCCTGGTCGAGGTCACCTGTCGTT<br />
CCCGTCCCCACCACTCACCAAGCGCTCCCAGGTTCTCCGTCTGGAAGACCCTCTGCAGCGGGGGGATGTA<br />
AATGACCGCCAGCTGCCCCAGGATGGACCCCAGGACGGAGTAGAGGAACATGTGGTTCCTGAGAAAGCCG<br />
ATCTCAAATATCAGCTTGGTCTGCAGGGAGAAGGTCACACGGGGGATTGTGTGCTGTCCACACCCCAGGT<br />
ACAGGCAGGGGAGCTCTGACTGCCCACGCTGAGCCAGAGCCGCTCAATGCTGCGGGCAGGGTCGGGGCGC<br />
TGCTGTCGAGAACACACAGCAGCTCTGCAGCGAGGAGGGTCAGCCCGGGTCTCACCTGAGAGCGGCAGGT<br />
CAAGGCGTTGAAGAGATCGAAAAACACAAAACAAGTGAACGTCATCGTCGTGGTGCGGGGAGTGCTTGCT<br />
CTGTCTTCAGGCATCTGGAAGGTGAGCACAAAGATGTGAGCTGTGGCAGGAGGGCAGGGACTGCAGTCCC<br />
CAGCGTCTGCACCGCACCAGGGCTTGGAGAACAGGCCGGGGTGACCCTCGCTCACCTCCTTCCAGAAGAT<br />
AAAGAGGGTCCCGCTGATGATGATGGCCGCGGACATGAGGATCTTCAGGATGAGGGCTCTGCTGAGGATG<br />
GTGTCCCGCACACTCCGTGGTGGCTGCCTGAAGGCGTCTTTGTCAACGGGCTCTACCCCCAAGCTGCTCC<br />
GAACAAGACACAGACACTTTGAAATGAACCAGGAATGAAATAAAGGACCCTTGAAACAGCTGTGCCTGAG<br />
CCTCCCAGGCCAAGTTGGCACAGGGGGCAGGGCCAGGCATTTGCTGAACGCCCCCAGGCATCGCACCTGC<br />
CCTCCTCGGCACCTTCCAGAAGCCCCAGAGCCTGGGTCCATGGGCAGCTGTGCCCCTCCATCTGTCCCGC<br />
AGACAGTGAAGGAAGACCACCCCGTAAGGCCAACCACACACAGTTCCATACACCCAGATGATCTCCATCA<br />
CCCCGAGGGGACCCCCCCCAACGTTGCGCCTGGAGAAACAGGCTCCAGGCTCCGCCCTCCGCAGAGCCCC<br />
TCATCAGCTGAGAGAGACCAGCCTCCAGCCAACTCCACACAGCAGGGTTGAGGCTAGACCCGCAGCAGGC<br />
GGTATGGTGGGAGTGGCCGGGTGAGGCCCTGCCGCTCAGACACAGCTGAGGCCAGCTTCCTGGTCCCACT<br />
TCTGCTCCCAGGGAGGGCTGGCAGGAGAGGTAACCCTCACACTTGGCTTTGGGGACACAAATGAGGACTC<br />
TCTTTCCCTTGGCAGCTATCACTGGTGATAACAGCAGCACTGAGCTCCAGCGGAAGCACTGGCTCTGTGC<br />
TCATACGGTTACGCACACGTGGCCAGATGGGTCCCCTGACTCCAAAGCGCATTCCTTCCCCCACACCACT<br />
TGGCCAGCTTGTTGAAGGGGATATTAAGTGGCGGAGCGGGTGGACTCCTGAGCACCTACTGAGTGGCAAG<br />
CCCTTTATCTCTAGACATCAGGGATGAAACACAAACTCCGCCTCCATGAAACTGATGTTCTAAAGGGGAG<br />
ACAGATCACAATCAGATCCATAAGGAAAAGTGTGTCTGTGTGTATCTTCCTCTCTAGGGAAAAATACAGC<br />
AGGGTGAGGGGATTGAGTGGGAGTGCAATCAGGGAAGACTTCCTGAAGGCAGTGACTGGTGACTGGAATG<br />
AAGCATGAGAATGAGCCATGCAGGTTGCCCAGAGAGAGCATCCAGGCAGAGGGAGCAGAAAGTTCCATCC<br />
TCACCCAGCTCTGCCGGCCCAGGTACTTTCTCCTCTGCCTTCTACTCCCAGTCTCACTGCAGTGCAACAC<br />
ACTTCAGTTTTCTGGGAACTCCTGATGGAAAGTGGCTGTATTTGTTCATCCCTATAGCCTTGGGGCACAG<br />
CCAGCAGCCCCTGGAGGAAGCCCCGCAGGTGGGTAAAGAGACACAGGGCTCCCAGCCGGCCCTGCCTCAC<br />
CTCTGCGCCGGTGGCCCATCCATGATGATGTTGATCCATAGGATCTGCATGGCGTTGAGGGGGCTGGGCA<br />
GGTTGAACACGGTGGACAGAGTGATGAGACTCAGGGCGGAGATGCTCCTGCGGGGCAC</dnaseq><br />
<br />
<br />
==Labs working on this lncRNA==<br />
*Department of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Li D, Zhang J, Wang M, Li X, Gong H, Tang H, Chen L, Wan L, Liu Q. Activity dependent LoNA regulates translation by coordinating rRNA transcription and methylation. Nat Commun. 2018 Apr 30;9(1):1726. doi: 10.1038/s41467-018-04072-4.<br />
</ref>(1)<br />
<ref name="ref2"><br />
Miao YY, Liu J, Zhu J, Tao YL, Zhang JA, Luo D, Zhou BR. The Effect of<br />
Botulinum Toxin Type A on Expression Profiling of Long Noncoding RNAs in Human<br />
Dermal Fibroblasts. Biomed Res Int. 2017;2017:2957941. doi:10.1155/2017/2957941.<br />
</ref>(2)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=LINC01021&diff=1276484LINC010212019-08-13T02:48:35Z<p>Qianpeng Li: </p>
<hr />
<div>==Annotated Information==<br />
===Name===<br />
Approved symbol: ''PURPL''<br />
<br />
Approved name: ''PURPL'' : p53 upregulated regulator of p53 levels<br />
<br />
Previous symbols: ''LINC01021''<br />
<br />
Alias symbols: LOC643401, RP11-46C20.1<br />
<br />
HGNC ID: HGNC: 48995<br />
<br />
RefSeq ID:NR_038848<br />
<br />
Ensembl ID: ENSG00000250337<br />
<br />
LncBook transcript ID: HSALNT0289082<br />
<br />
===Characteristics===<br />
''PURPL'' is a p53-dependent transcription driven by a MER61C LTR. CMS4 tumors with low ''PURPL'' expression were associated with poor patient survival<ref name="ref1" />.<br />
===Function===<br />
<br />
* ''PURPL'' contributes to cellular survival in response to genotoxic stress by suppressing apoptosis<ref name="ref1" />.<br />
<br />
===Regulation===<br />
''PURPL'' is activated by P53 in colorectal cancer (CRC)<ref name="ref1" />.<br />
===Diseases===<br />
Colorectal cancer (CRC)<ref name="ref1" />. <br />
<br />
===Expression===<br />
In CRC patient samples, ''PURPL'' expression positively correlated with a wild-type p53-associated gene expression signature. ''PURPL'' expression was increased in primary colorectal tumors and displayed a bimodal distribution that was particularly pronounced in the mesenchymal CMS4 consensus molecular subtype of CRCs<ref name="ref1" />. <br />
<br />
<br />
===Evolution===<br />
-<br />
===pubmed IDs===<br />
26183718, 29262524<br />
===Sequence===<br />
>gi|336391099|ref|NR_038848.1| Homo sapiens long intergenic non-protein coding RNA 1021 (LINC01021), long non-coding RNA<br />
<dnaseq>CTGGGAATCAATGTGTGAGGTGGTGCTATGTAGCAGGAACCCCTCTTGCTTTGCAAATAGTTTTTTGTTTGTTTTCCTTTTTGCCCAATAGAGCCCTGCTCTACTGACCCTTCAATGTGCCCGTGTGCCTAAATATTCCTGGTCGTGTGAAAAGAACCCAGGTATTAGCTGAACTAAGGAGCACAATTCTGCAACATTTTGGCACCCAAACACGGGGCTTGAGAAATGAATGCAATTGGAGAAACTGGTTGTTTTACCAGGCGTTGATTGGAAATGTGTGCTTCCCTTTAAGCAGTCAAGCTCAACTTGCAGAACTGATGGGAACCCCTTGGGAAAACTGGCCTCAAATGTTTGTCTACACAGTCCACATACAGGGTTCTTAACCTGCGATGAGGGAAACTTCCCAGGGCTTGTCTGGGTATGCCCACAGTGGACTGGAGCCCAAAATGCACACTGGAGGAAGTGGATGGAGCCACGTGGATGTCATGCCTTATGCAGGGGAGGAGCCTGCTCTCTTCAGCTCCTGTGGTAATGTGGGAATCGATCTGTGAGCATATTTAACTATCCGGCTATTTTGGAGATTGAAAAAAGAAGACCTGATTTATCATGTGCAATATCTCACACATCTGTCATTTCTATTCTACCGCAATTCGATGGAGTCTTGTTCTGTGGTCCAGGCTAGAGGGCAGTGGCATGATCTCGGCTCACTACAAGCTCTGCCTCCCGGGTTCACGCCATTCTCCTGCCTCAGCCTCCTGAGTAGCTGGGACTACAGGCGCCCGCCACCACGCCTGGCTAATTTTTTGTATATTTACTAGAGATGGCTAGTGTTAGCCAAGATGGTCTCGATCTCCTGACCTCGTGATCTGCCCACCTCAGCCTGCCAAAGTGCTGGGATTACTGGCGTGAGCCACCGTGCCTGGCCAGCATCCTCTAATTATTATTCATAGTTTGTGAATTTAGGCCTACGTGAATAATAATATAATATTTACTATGATGTTACTATCTACCAACCTTATTTTTCTTTTCTATAAAATAGGAGCCAAAATAATATTTATGTCATACCTTATGAAGTTAAAATAAAATATAACGAATGAGGGGCTTAAAAAAAAAAAAAAAA</dnaseq><br />
<br />
==Labs working on this lncRNA==<br />
* Experimental and Molecular Pathology, Institute of Pathology, Ludwig-Maximilians-University Munich, Munich, Germany.<br />
<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Kaller M, Götz U, Hermeking H. Loss of p53-inducible long non-coding RNA LINC01021 increases chemosensitivity[J]. Oncotarget, 2017, 8(61): 102783.<br />
</ref>(1)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=VIM-AS1&diff=1276483VIM-AS12019-08-13T02:47:55Z<p>Qianpeng Li: </p>
<hr />
<div><br />
==Annotated Information==<br />
===Name===<br />
Approved symbol: ''VIM-AS1''<br />
<br />
Approved name: ''VIM-AS1'': VIM antisense RNA 1<br />
<br />
Alias symbols: -<br />
<br />
HGNC ID: HGNC: 44879<br />
<br />
Ensembl ID: ENSG00000229124<br />
<br />
LncBook transcript ID: HSALNT0159506<br />
<br />
===Characteristics===<br />
VIM-AS1 was reported as one of the optimal predictive lncRNA biomarkers of UCEC progression<ref name="ref1" />.<br />
<br />
===Function===<br />
* ''VIM-AS1'' promotes tumor growth and metastasis by inducing EMT in colorectal cancer (CRC) cells<ref name="ref2" />.<br />
<br />
===Regulation===<br />
-<br />
===Diseases===<br />
Endometrial cancer<ref name="ref1" />.<br />
<br />
Colorectal cancer<ref name="ref2" />.<br />
<br />
===Expression===<br />
''VIM-AS1'' transcript was significantly upregulated in high-grade, lymph node metastasis and vascular invasion tumors<ref name="ref2" />.<br />
<br />
===Evolution===<br />
-<br />
===Sequence===<br />
>NR_108061.1 Homo sapiens VIM antisense RNA 1 (VIM-AS1), transcript variant 1, long non-coding RNA<br />
<dnaseq>TTCTCCCGGAGGCGCATGATGTCCTCGGCCAGGTTGTCGCGCTCCACCTCGACGCGGGCTTTGTCGTTGG<br />
TTAGCTGGTCCACCTGCCGGCGCAGCTCCCGCATCTCCTCCTCGTAGAGGTCCCCCAGGCGCGACTTGCC<br />
TTGGCCCTTGAGCTGCTCGAGCTCGGCCAGCAGGATCTTATTCTGCTGCTCCAGGAAGCGCACCTTGTCG<br />
ATGTAGTTGGCGAAGCGGTCATTCAGCTCCTGCAGCTCCACCTTCTCGTTGGTGCGGGTGTTCTTGAACT<br />
CGGTGTTGATGGCGTCGGCCAGCGAGAAGTCCACCGAGTCCTGCAGGAGCCGCACCCCGGGCACGCTGCT<br />
CCGCAGGCGCACGGCAGAGGAGCGCGTGGCATACACGCCGCCCGGGGACGAGGCGTAGAGGCTGCGGCTG<br />
GTGCTGGGGCGCAGCGCGCTGCCCAGGCTGTAGGTGCGGGTGGACGTAGTCACGTAGCTCCGGCTGGAGC<br />
TCGGCCGGCTCGCGGTGCCCGGGCCGCCGAACATCCTGCGGTAGGAGGACGAGGACACGGACCTGGTGGA<br />
CATGGCTGCGGAGGGTGGCGATGGCCTGGGCGGCGGCGGTGGCGCGGACTGGCTCCCGGAGAAGAGGCGA<br />
ACGAGGGCGCGACAGCAAAGCTCCCTTTGGATGACATAGATTTATTACTTAGTAGTATATTATGTATTGG<br />
CTGTCCCACATTTTGAAATTTAATGGACTCGTGGTGATCAGAATAAAAGAAGCCTTCGATGTGAGGCCCA<br />
GGCATTGAGTACCATGTGTGCGATTCACAAGCCTTGGCATCTGAACAATTTTTTGGAAGGATCCATCAGG<br />
ACAACACGTCGGGGGTGTACTAGTGAAGTGATTTTCCAAATGTGCTACTCAGACCTGTAGCATCAGCATC<br />
ACCGGATAATTTGTTAGAAATTCCAACTGTTAGGCCCCACTTTAGACCAACTGAATGTGAAACTCTGGGA<br />
GTACGTGGGGCCCAGCAATTTGTGTTTTTACAAGACTTACCAGGTGATTCTGAGAACCACTGTGCTAGTG<br />
AATTGTTCCTGTCTGTGGCCACGTAGAATAAGAAAACCATAGGGTTGGAAAATGGGGAAACTGGTGAGTG<br />
TTCGCTTATGAGGAAATGAAGAATAGATAGAAAAGAATTAGTTAACTTTTGGAATTCAAAAGAGAAGCAG<br />
TTTGTAAAAGCCAGGAATTTGATTTGAAGGACTAATTGCTTGCAGAATCTTTGCTTTCTCAGAGAGGGGC<br />
AATCCAGATCACTAGGTTACCGTGAAATATGTTGGTATGGCTCTAAAATTCTAGAATAATCTCTCTAGTG<br />
AGAAAAGGCATACCTTTCCATATTAGGACAAAACTTCAAATCAGGTTTGTAAAATCCTATAAGATTATTG<br />
TATCCCATTGCCATGGCCAACTTGTTTGTCTCTGGAGATCCCAGTTTCTACATCTGAAAACCATATGCAT<br />
TCCTGCTCACCAGGAATTATCTCGCTGAATGAAGCAAGAGATTCAGGATGTGTAAGAGAATTTATGAAGC<br />
ATTTGGATTACCAAGAAATGTGAAGTATAAAGATCAAGAATGATTATTACAAACACTGATGGTAAAGAGG<br />
TGTTTCGAAGTCGATGCAAAAAATGAGTTGCTTATTTCAGTCTCTCTTTGATATATCTGCCTTTTTAGTG<br />
CTGACTCTATCATGTATTCACTATTTGATTTTCAGTGAATCACATTTTTTAAAGCTTTTAATCTGTTTCC<br />
TCAAAAAATATATTTTTTAAAAATATTTACTCAGGATTGTTGTGAGAATAAAATTGATTCGATTGATATT<br />
TCAAAAAAGAAATATATTTTTAAAAAATAAAGCAATACCATTTTTGGATATGCTAAAAAAAAA</dnaseq><br />
<br />
==Labs working on this lncRNA==<br />
* Department of Biotechnology, Institute of Science and High Technology and Environmental Sciences, Graduate University of Advanced Technology, Kerman, Iran.<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Sun Y, Zou X, He J, et al. Identification of long non-coding RNAs biomarkers associated with progression of endometrial carcinoma and patient outcomes[J]. Oncotarget, 2017, 8(32): 52604.<br />
</ref>(1)<br />
<ref name="ref2"><br />
Asadi M H, Yaghoobi M M. Long noncoding RNA VIM-AS1 promotes colorectal cancer progression and metastasis by inducing EMT[J]. European journal of cell biology, 2018, 97(4): 279-288.<br />
</ref>(2)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=MIR4697HG&diff=1276482MIR4697HG2019-08-13T02:47:04Z<p>Qianpeng Li: </p>
<hr />
<div><br />
==Annotated Information==<br />
===Name===<br />
Approved symbol: ''MIR4697HG''<br />
<br />
Approved name: ''MIR4697HG'' : MIR4697 host gene<br />
<br />
Alias symbols: LINC00947, LOC283174<br />
<br />
HGNC ID: HGNC: 27448<br />
<br />
Ensembl ID: ENSG00000280237<br />
<br />
LncBook transcript ID: HSALNT0289513<br />
<br />
===Characteristics===<br />
<br />
===Functions===<br />
* MIR100HG, LINC00340, ''MIR4697HG'', LOC401093 are up-regulated in GC samples compared with their paired normal tissues and correlated with shorter survival, indicating a detrimental role in GC biogenesis<ref name="ref1" />.<br />
<br />
* ''MIR4697HG'' promoted ovarian cancer growth and metastasis. The aggressive role of ''MIR4697HG'' in ovarian cancer may be related to the ERK and AKT signaling pathways<ref name="ref2" />.<br />
<br />
===Regulation===<br />
<br />
===Diseases===<br />
Gastric cancer<ref name="ref1" />. <br />
<br />
Ovarian cancer<ref name="ref2" />. <br />
<br />
===Expression===<br />
''MIR4697HG'' is up-regulated in Gastric cancer(GC) samples compared with their paired normal tissues<ref name="ref1" />.<br />
<br />
Transcriptional level of ''MIR4697HG'' in cancerous tissues increased twofold compared with that in adjacent noncancerous tissues. ''MIR4697HG'' was differentially expressed in ovarian cancer cell lines, with the highest levels in OVCAR3 and SKOV3 cells<ref name="ref2" />.<br />
===Evolution===<br />
===Sequence===<br />
>NR_024344.1 Homo sapiens MIR4697 host gene (MIR4697HG), long non-coding RNA<br />
<dnaseq>AGGAGACCCTCCTTTGTTTGGCTCTTTTGCTAGACAACTTCTGTTTGGGTAGGAGGGTCAAATTAGTAAT<br />
GCACCATCTTTAATGTATTTTTTATGGAGACTGTACATAAAATTATATAAATCTACAGAATTGGTTCTAT<br />
TTTAAGGAGAGAGGGGAATGTATGTGGGAGGCAAGGATCAGATGCAATCGTGGAGACTGGGAGCTTCGGG<br />
CGAGTGGCACTCGGGTGTGGGGAGCGGGAGGGCAAGAGATGAGTGCCGGGCAAGATGGGCAGGGGCCCGT<br />
GCCCTCTGCACACATATATAAATATAAAGAACACCTAGATAAAGTCTATATATCTCTATATCTATATGAA<br />
GTCATAGTTTGCTTTATTTTTGTACCTGTGCTTAGAGATGTTTTGAGCAGTGCTACCTTCCCAGGCAGTC<br />
TGGGATACTAGCTCATGCCTTGACGCCACCTCCTTCCCTGCTCTTCCTTTGGTATTCTCTCTGTTCAGAG<br />
TTGCTTGGGTCTTTCTGATGGAAATGTGTATATATGAAAAGTTTGTAAAATAACAAAACAAATAACCCAC<br />
CTGCAGGAAGGACAAGTGAGCTGAAGGTTGTGTGGAGCTGCAGGATCTGATAGCCCTAAAGAACCAGGAC<br />
CAATGTGTCTCTTGCCACTTGGGAGGGATGTTGACTTGAACTTCTTTGCAGAGGGGCTTAACAGGGCAAG<br />
GCTGAGGAGATGAAAACTGTGACTCCATCCCCACGTGGCTGTGGAAAGGTAACCAGTTCCTCAGAGAAAA<br />
CCTGGCTTCACAGCATTAGAAAGGGGGTGGTTGAGACTACCTAGGGACCTACGGTGACACCTGTCTTGGT<br />
TTGTAGCACTGTAGCTCAGACAGCTCAGACCGCTCATAGAGGGCATGGCAATGGGAGAGTTTGTGAGGCT<br />
GGCTGCCTGGGCTTGGTCTTGGAGAACACATGGCCTGTTTAGTGTTGCTGCAGATTCTTAGAGCCAGTGT<br />
GAATGTGGTATGTAGTATAAATATGTCATCTATGTTTTTTTCAGTTATTTTTAATTGGAAATAAAGTGCC<br />
ATTGCAAATAGGATGCTCCAATCCTGGGACACTGAGTGGAGGATGAGGAGGGAGAGATGAACTGTGGGCC<br />
GGCCTGGGAGAGGGGGTCTTAGTGGAACCTTCCTTCTGGCCTCCAGCCGGGGACTTACAAAACTGAACAA<br />
TGTATTGGCAGAACTGGACCCACAATGGGAGATTCTGGGGAGCAGGAGTTCACTTGTATCTGAGCAGGAA<br />
GCAGTGTGCCCTGAAGAATACCTCTCTGAGCAAATTCCAGACCTCACACATATGCAAGGGCTCTGCCTTG<br />
CAGCCTCAGCAAGCGTCTCCTGGTGCTAGCTCCTTCCTGACTTGCCCGGAGCTCGGAGTGATGTATTTGA<br />
AGCTGGTGCTGGGCCAGATGGTGCAGGCAGTGAGGAGAGACTCAGGACTGCAACCTTTCGGCTCCTTATT<br />
CCTGCTCATCACTCAGAAAAGGGCAGTACTAACCCCTTTCCTAACCAAGACATGGCACTCCCTAAGAGCT<br />
CTTGTCTATAGAGTTTGGTCCTTAGAGGAAAGCAGATACCTTCAGCGTGAGAAGGGCTTGGTTGACAGTT<br />
TTGGGGTATTATGGGAAGAGTAGGTTGGGGTAAAGCTTGAGTCTAACTCTTGATCCTTACATGGACCTAT<br />
GAGGCCCTGCCATTCAGTCAGGCACTGTCCTTGGGTCCTCAAATTAACTGCTGAGAACACTCCCCACTTT<br />
CCGAGGACGCTGATGGGAAATGGGCTCTGTCCATGCAGCTGGAAGGATCCAGTGCTGGTGCCACTGTCAG<br />
TGGCACCATCCTTGCCTTGAATGATCTTTCTTGCAGGCTCCTGCAGCTGAGTGTTTCTTGTAAGATTTTT<br />
CAGGGGGATTGGGCAAGAAGAAGAGGTGCAAATTCTGTTCCCTTCCTACCTTGAAGCCTTCCCAGACCAC<br />
CACGGTCTCTGCACAAGGGAGGCTCCCATTACTGTTCTGTTGGCTTCTAGACCCACCATCCCCTCTCTTT<br />
CTGTGGACTCTGCCCGACTTCTGGCCACATGCAACCAGCAGAGTAAACTGCTCCAACACCTCGGGCATGT<br />
CCTAGGGCTTGCCCTCCCACCAGGGCCAGCCCAAGATTAGGTCCTCAGCAGCATCAAGGTCTGGGAGAGC<br />
CACTGGCCCACATGTCACCATTCTATTCCTCAGCCTCCAACAGGACTCTTCATTTTGGGGAGGGAAAGGG<br />
AAGATGGGGCCATAGCCCCTACCTTGAAATTGTACAGTGTGGAGGGGATGTTAGTGCCTACCTGTGACCT<br />
TTCTGCTCCACTGCTCAGCAAGATGAGGTAAGGTTGGGTGTCAGAGGGGACCTCCAGCTTCTCTGAAGAG<br />
CCAGCCCTTAAGGCACTTGGAGCAAAGGTCATTGAGATCAGCTTTATGTGGAGTAAGGAGGAGGCCTGGG<br />
AACCGCTTGTGGCATCAGTTGGGGCGACAGGTGGATGAGTGTGCTCTGATGGAGCTTTTACGGCCCACAG<br />
CCACTGCCAGGAGCCTGAGCTCTTCCCCATGCTTGGGACACGTTCCTTGGTCCCCACAGCAGAATGGACA<br />
TTGAATTTTGGTGCTTTTCCCTTTGGTAGAAGGTGGAGGTATCTGAGGAGTTGTTTCTGTCTTGCTACCT<br />
CTGTCTACTATATAGAGCAAGAGTCGGGAATAGGGAGATGTGTGAGAATCACTCTCCCATGGATCAGTGT<br />
GGGCCCTGTCCCTCTTCCCCACTGTCACCAACCAGCAGCTTGGGGAAAAGGCTCTGTCGTGGATTTTTGC<br />
TGCCTGCTTCCCGCTTCCACTCTTCTTGGCGGTAGATGTTCATGGTGATCCACTTTGGGCGGTCTGAAAG<br />
TAGGAGGTGGGGGAAGAGGCAAGCCTGCACACACACTTCCTGTCCACAGGGGGTTGCCTGTGGCATTGGA<br />
GGGTGGAGTCTCAGAGTCCAGGGACTGGGAGGAAGGTACTTGATGGGATGGTCTTGATTCTGGAACTTTA<br />
GACTGAGGTGTTAGAAAGGGGAATTGTTGGCTAGGGGAGAAGAGCAGTTTAACGCTCCACTTGCTAAGTC<br />
GTCTGTATCAGTGTCAGAAGGTCTTGACCTCCCATTCAGATTTAATTTCCTAACTGCCAGGTGTGGGGCT<br />
GGGGATAGAGGGCCCAGAAGGGGGCGCAGTCACTGACGTGAAGGGACCACATCCCGCTTCATGTCAGTGA<br />
CTCCTGCCCCTTGGTCTTCAGTGTTTTTCTCTTCCCCAGGAGGGACTTTGATCATGCAGGATAGAATTCT<br />
CCCATCGCACACCTGGGGGCAAGTTTTAGATGAGCTTCTTTCCTCCATTTCACCTGGTGGTCTGAGGACA<br />
CACAGAGGGTGGGGGTGAGCAGGCAGTGTGGGTGGGGAGGGGCTACCTCCCCCAGACCCCTTACAAACTC<br />
TGTACCTCTCGGTGCGCGGCAGCCTCTTGCTGTAGTTCTTCTTTTCTGGATATGACTGTCAGTTTCGTCA<br />
TGAGATTTCTTGCTCTCATTTCGAACTCTTTCTTTCTTCCACTTTCTTTGGGGGCGACCCCCGATCCATG<br />
CCAGGTCTTCCTGTGAAGACCGTTCCAACCTCGTTTCCATTTCTTGAATGTTGAGTATTACAACATCACT<br />
GCGCTAGGGTGCTTCATGGTGCTGTTCTCGAAGAGGCCAGTTGGGCTGAATCTCCTTCCTCCCACTGGCT<br />
CCTGATATCTTGCTGTATTTTGTCTTCTTTCTGATTTTTCCCTAGGGGTTTGGGGTGGGTGACTTAGGGG<br />
CGGCTTTTGTGTTCTCCCTCTCTCTCTCTTTCTTTTCTGTATGTATGTATGGACTGGTTAAAGTGAGTTT<br />
GGGCAGCTGACTTTATGGTATGGGTTGGCTGACTTTTGTTCAACATTAAAGACAAACCAACAAATTGTAC<br />
AGCTGCACACAGAACACCTTTGAGTGTGAACTTGAATGGCAACTAGAGGCTTACTTTTTGAACTTCAGGT<br />
ATGTAACTCAAAAGTAAATAAAACCACTATTTTTTCAGTAAGCTTTTTTTTCTTCTAAAAGATGACTTAG<br />
AAATCAAACTATAAGAACATGAAATCGGTGCTGTACCAAAGCCTTATATGAACATATTCTACACTCTGTA<br />
TAACCTGTCTGTGAGGAGCTCCCTGCTCTATCACCCTCTTCTCAAAAGCCTGGGAATGCCAGCGCGTGCC<br />
AAGCCTGGGGCTGGGTCTTGGGGACCTGTGGGCCAAGGGCACCCTGGGAAGTAAAAGATGACGGTGAGGA<br />
TGGGACACCCTTCTGCTGCCTGAGCAGACTGCAAGGAAACCAGATGTGTGTGTGTGCGCGCACCTGCATA<br />
TATATGTGTGCATACCTGTGCGTGTGTGTGCGTGTGCGTGTGTGCACGCAAGAGAGTGAGAGCGGGAGAG<br />
AGCTCACAGGTGCACAGTGTCATGGTGAATGTACTAAGTACGAGCTTGAAGGGAGGCCCAGGTTGGCTCT<br />
GGGAGTGGGGCGGTGTGGGAATGAAGGGGGGATGCTCTCTCCCCTGTTTTCTGCCTCCTTCCCTTCTCCG<br />
TCAGGGAAGGGAGGTGTATTGGAAACAGCTACACTCTCAATCAGGTGCTTTTTTTCCCTCAAAATCTCCA<br />
AACTCAAAGCATTTATAAGGGGCCCTTCCAATGGGCAGGCACCCCCAGCCACCAAATCACAGACTTCCAA<br />
GAGTAGGAGGAACTGTCTCCTCCCGAACCCTTCCTTGCTTTCCTGGGGAAGAGGGTTCTTCCTGCAGGGA<br />
CCCTGGGCATCCTGCTGCTGGGCCTGGGCCTATAGACTGCCCTGCCCCTTCTTCCCAAACACTGAGAAGA<br />
CCCCGCTGGAGATGACCCCAAAGCCACGCCTGCTCTACGGCCCTAAGCAATAGACGCCTGCCCTGGCTGC<br />
TGATGATGGTGATCCCTTTGTCCTTTGACTTGGCAGTCAAAAATGGAGTGACACCCCAGACTCAGTCAGG<br />
AAGAGAACCTGCAGCCTGCCTCAGCTCAGGCTACCACGCCAGGCTCCACTCGCTGGTATTTCCAGGCTTG<br />
CTAAGTACTAACCAACTCATCCCCAGTAACACTGCATGTTCATATCCTGAATTACAAATCAAAATGAGCA<br />
AACACGTGCATAAGCAAATGAGAAAAAAGAAGGCACACATCAAATGATGAGATGTGCAGCCAGTGCAGGT<br />
ACCCCGGGAGTGTTGCAAGTTAAACTGATGAAAAGACGTTTAGTATTTAATTGCTCCTCATGTAACATTA<br />
CTCTGCTTCAGAAATGTTTTGTATTTTGATATAAATAAACATTTGCTAAAAAAGTT<br />
</dnaseq><br />
<br />
<br />
==Labs working on this lncRNA==<br />
<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Tian X, Zhu X, Yan T, et al. Differentially expressed lncRNAs in gastric cancer patients: a potential biomarker for gastric cancer prognosis[J]. Journal of Cancer, 2017, 8(13): 2575.<br />
</ref>(1)<br />
<ref name="ref2"><br />
Zhang L, Yang S, Wang Y, et al. Long noncoding RNA MIR4697HG promotes cell growth and metastasis in human ovarian cancer[J]. Analytical Cellular Pathology, 2017, 2017.<br />
</ref>(2)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=LINC00968&diff=1276481LINC009682019-08-13T02:46:29Z<p>Qianpeng Li: </p>
<hr />
<div><br />
==Annotated Information==<br />
===Name===<br />
Approved symbol: ''LINC00968''<br />
<br />
Approved name: ''LINC00968'': long intergenic non-protein coding RNA 968<br />
<br />
HGNC ID: HGNC: 48727<br />
<br />
Ensembl ID: ENSG00000246430<br />
<br />
LncBook transcript ID: HSALNT0289073<br />
<br />
===Characteristics===<br />
<br />
===Function===<br />
<br />
* ''LINC00968 '' acts as oncogene in NSCLC by activating the Wnt signaling pathway<ref name="ref1" />.<br />
<br />
* A bioinformatics analysis reveals that there is a ''LINC00968'' /miR‑9‑3p/CCNA2 regulatory axis in lung adenocarcinoma<ref name="ref2" />. <br />
<br />
===Regulation===<br />
<br />
===Diseases===<br />
Non-small cell lung cancer<ref name="ref1" /><ref name="ref2" />. <br />
<br />
===Expression===<br />
<br />
<br />
===Evolution===<br />
<br />
===Sequence===<br />
>NR_038236.1 Homo sapiens long intergenic non-protein coding RNA 968 (LINC00968), long non-coding RNA<br />
<dnaseq>ATGTTTGCCAAAGAGTGCAAAGTTTCAGTTACATGGGAGGAATCAGTTCTGGTGGTTTATTGCAAAACAT<br />
GGTGACTATAGTTAATGTACTATGTATTTCAAAACATCTAAAAGAAAAGATTTTAAGTGTTCTCACTACA<br />
AAGCAATGATAAATATTTGAGATGCTGAACTTTTTAATACTTACATTCTTAAGTTTTTCAAGGCTTTTCT<br />
AATAAGTCTGGCATTCCTGCCCTTGGCAGTGTGAGATGGAAGATGATGTCGCAAGGGTGGCCGAGAAGCA<br />
GCTGGGCTGAGCTGCTAAAAGCACAGAGACCGGGGCCAGACTCCTCAGCCTGAAATCCTGCTTCCACTAA<br />
GTACCAGCTGGGTAACTTCAGGTGGAGCCCAGTTGACAGGAAATGTTTCTCCAGAAGCTGAAAAGCTGCC<br />
TGGTAAAGGCCTTTCATAAAATGGTCTGCGTTTGGGACCAGGAAGACAGAAGACTCCTCAAGAAGAGAAC<br />
TGGAACCTTAACCCACTTCAGACTTCTTCATGTCTGAAGCTTATTTCCACCATCCCATTGAGAACCAAAG<br />
AAGCGAGCTCCTTGGAGAATCGGCTCCCACCTGGACCTTCTGTTTATCCTTCCAATAGCTGCTGCATTCA<br />
TCCTTCCCAGCTAATGACACTTCCAGCCTTTCGTGTTTCAAAGTATCACGGACTTTGCAAAAGATTCCAG<br />
GTTTCTATGGAGCAGATAGTACTTTTAACAATCAACATGTGCATTATTATTTCCTCCTAAGGCATACTTA<br />
GACATCAATGCATGCTACAGCAAGGCAACTTATCTCACCCTCACCAAGATATTCTGCACTTTCAGTGGCA<br />
AAATTTTAAAGAAAAGGAGACAAAATGGAACACAAATTCAATATGACTATTGTCATCCTTCCCTCCCAGG<br />
AAGTGTAGGAATCATCCAAAGTGGTAAAAGAGCAGCGCTTCTAAACTCTGACTTCACATGGAAAATAACG<br />
CGACTACTAAAACTGATAACAATAGCAGTCCATGCCATTTGACAGGGGTGTGTAGGAGAGGTGGTGAGCA<br />
AGCTGAAATCCCTTCAGGTATTTGCAGAACTTCTGAGCAAAAGCTAAAGCTAAAATTAACATTAAATATG<br />
CAAAGTATTTTTAACCCAACATAAATTAACAATGTTCCTATTTCAATTCTATTGCTCTTGGGATGACTAT<br />
GTCCTTTGGAAAATGTTTAAATAACTTAAGATTTCCGTCATGAGTTTACTATTTCAAAACTTATTTTTTT<br />
AACTGCAAGATACCTTTTTATGTTACCAGGAGTGTTACCAGCTAGCTGCCAAAACCTGGTTGAAGTTCTC<br />
CCACTTTATATTGTAAATGATTACATAGTTTATTAGTAATTGTGTCCCCTGTCCACCCACTGGTCCATTT<br />
GGATGGGAAAATTTTCAAAATAACTTCATAAGAAAATGATAAGAAAAATGTGGTCACCGGTATCATGAGG<br />
AACTTCCAGACAGCTCAGCACAGAAAAGTTGGTTTTAAAGTCCTCGAAAACGTTACTGGTAATGAGCTTC<br />
CACTCCTTTAGTCGTTGTGCATAGATACACCACAGAGTAAGGTTATAAAAATAAAAGTTGTTTCAGGAAA<br />
TTTCCCATTGCTTTATTACATGATCAATGAGAGTAAAGAGAAATGGAAGTTGACGGGATAGGAATGAGGG<br />
ACCTGCTGGAAGAGTGATCACAATATCCAAAGGAAATTTAAAATGCCTGTTGAAAGTGACACACTGACTC<br />
AGCATTGTCACTAACACAGAATCACCACAATAAAACTGCCCTGCCCTGTGGCTCCTGGCACCTCATGTCT<br />
CTTTAGGTTAAGCAGAGAGAGGTCTGTGTTGCTTTGGAACAAGGTGCAGCCTCCCCCTAAGCTACAGAGA<br />
GGCTCTGAGCAAGGACCAGCCCCCAGGGTGCAGCCTTGCCCACCCTCCACAGGCTCCAGAGCAGATGGGG<br />
TGGCTCTAGAGAGCAAATGGTCAAAACTTCTAGCGCTAAATAGAGCTTTAACATGTCTCAGATACTAGCA<br />
AAATAGAGAAGCCTCAGATGGCTTTAGGTCTGGAAGTGTGTTGCTAAAAATGCTAAAAATTTAACAAACT<br />
TTTATAAATCCTTAAGAGATCTTTTTCAGTTTTCTGAAGTACCGTTAATTGCCCATGTGTTTCAACTTGC<br />
AGACAGGCAAGAATTTGGCTTTGTATGTTTAAAAATATGTACATCTTGGTTCATAATGATGATTTATTTC<br />
CAAAATGGTGACTCATACTAGGATTACATATAAAACATCATATGTGGGCCTTATATGTAATAATGTGTAA<br />
GTATAGTATATTAATTACTCTGACATAACATGGGCAGAGATTTGTATTAATTTATTTCTATTTCATCTAA<br />
TCAATATTTTACTTAAGTCTAAAACCTTATATATATATTGACATGTATCATCGTATATATAAACATTGTA<br />
TCTATTGAACTGAGCAATCTGTAGTTTATTTTAAATTCTGATACATTAAAGATGTGGAGAACTACATGAA<br />
AAAAAAAAAAA</dnaseq><br />
==Labs working on this lncRNA==<br />
<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Wang Y, Zhou J, Xu Y J, et al. Long non‐coding RNA LINC00968 acts as an oncogene in NSCLC by activating the Wnt signaling pathway[J]. Journal of cellular physiology, 2018, 233(4): 3397-3406.<br />
</ref>(1)<br />
<ref name="ref2"><br />
Li D Y, Chen W J, Shang J, et al. Regulatory interactions between long noncoding RNA LINC00968 and miR‑9‑3p in non‑small cell lung cancer: A bioinformatic analysis based on miRNA microarray, GEO and TCGA[J]. Oncology letters, 2018, 15(6): 9487-9497.<br />
</ref>(2)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=LINC00941&diff=1276480LINC009412019-08-13T02:45:46Z<p>Qianpeng Li: </p>
<hr />
<div>==Annotated Information==<br />
===Name===<br />
Approved symbol: ''LINC00941''<br />
<br />
Approved name: ''LINC00941'': long intergenic non-protein coding RNA 941<br />
<br />
HGNC ID: HGNC: 48635<br />
<br />
Ensembl ID: ENSG00000235884<br />
<br />
LncBook transcript ID: HSALNT0289072<br />
<br />
===Characteristics===<br />
<br />
===Function===<br />
* Depletion of lncRNA-MUFs in HCC cells repressed EMT and inhibited their tumorigenic potential. Conversely, lncRNA-MUF overexpression accelerated EMT and malignant capacity. Mechanistic investigations showed that lncRNA-MUFs bound Annexin A2 (ANXA2) and activated Wnt/β-catenin signaling and EMT. Furthermore, lncRNA-MUF acted as a competing endogenous RNA for miR-34a, leading to Snail1 upregulation and EMT activation<ref name="ref1" />.<br />
<br />
* lncRNA LINC00941 is a crucial regulator of human epidermal homeostasis. LINC00941 acts as a repressor of keratinocyte differentiation. Furthermore, LINC00941 represses SPRR5, a previously uncharacterized molecule, which functions as an essential positive regulator of keratinocyte differentiation<ref name="ref2" />.<br />
===Regulation===<br />
<br />
===Diseases===<br />
Hepatocellular cancer<ref name="ref1" />. <br />
<br />
===Expression===<br />
<br />
LINC00941 is enriched in human progenitor keratinocytes<ref name="ref2" />.<br />
{| class='wikitable' style="text-align:center"<br />
|-<br />
! | Experiment<br />
! | Forward primer<br />
! | Reverse primer<br />
|-<br />
| rowspan="1"|Quantitative real-time PCR<br />
| | 5'-GACCTTTTCAGGCCAGCATT- 3'<br />
| | 5'-ACAATCTGGATAGAGGGCTCA- 3'<ref name="ref2" /><br />
|}<br />
<br />
===Evolution===<br />
<br />
===Sequence===<br />
>NR_040245.1 Homo sapiens long intergenic non-protein coding RNA 941 (LINC00941), long non-coding RNA<br />
<dnaseq>GGGGACGTGGCTGAAGTCAGTCGGGCCGCCCGCTTGCTGCACGGCAGCCGTGGGACTGGCACAGGCTCCT<br />
CGGCAGCATTATGGGCAGCTGGTAGAGCGGCCACTTCTGAGAGCCGGATGGGCCTTCCGAGGTCGGGCCG<br />
TGCCCCGCTGGGCAGCGCAGAGGGGGTGTGTAGGGCACGCGACTTGGAGCCAGGTCCAGACCCATCCTGG<br />
CTCCTCTCAGGGCTCCTTCCCCTGCCCCCATTCCACCCCAGCCCTGCTGGCTGTCCCGCAGGACCCAGCG<br />
CCGCGGTAGCCTTCTCTGAACTGCGGCTCAGGCGGAGGTGTCACTCCTGCCTCCAGCCCAGGAGGGCAGG<br />
TCAGGTTATGCAACGCGTGCCGCGCGATCTCCCCCCACCTCCAACCCCCTTTTCTCCCGGGTCCACACCG<br />
CAGTTCCCACCGCTCCGGGTGTCCTCCCCAGTGCGCCGCGATTTTTGTGTCCAAGCCCCAGAGTCCCTCT<br />
GAGACCAACCCCCAGCCAGCACAGACTTCCTGCCTTCCCAGCTCGGGGATGTGGTCTCATTAGGTTGCCC<br />
AAGCTGGACTTGTACTCTTGGCCTCAAGAGGTCCTTCCATCTCAGTCTCCCAAGTAGCTGGGACTACAAG<br />
CATGCACCACTACACTCAGCCAAATACTTTCAATAATTTGCCAGCTGACAACTTGATTGGGTTCTCCTTC<br />
AGGTTTGAAGCGCCCTCGAGAAGTGTCTAAAGGAGACAGTTGATAGCCAAACAACAGTTTTGGATTCACT<br />
GACTGATTATGAAAGAAGCAGTAGACTGGTATCAAGAATCAGTCAGCAAGGAGGCCCTCACCAGACGCCA<br />
GTGCCATGTTCTTGGACTTCTCAGCCTCCATATTCATGAACTAAGTTTTTGGAATCCTTAGGCTTCCACG<br />
TGTGGAAAGCCTGAGCTAACCTACTGGAGGATGAGCCATCACCTGGAGCAGATTCAGGCCATCCTAGTTG<br />
AAGCCTCCCTAGGCCAAGCAACCGTCCAACTACCAGACATTGACCATTCAGCCTTGAACATTCAGCACAA<br />
AGACAAAACAGACCAGACCAGAAGAGTCCCACAGAATAGGGGAAACTATTCAGAGAAAACTTAAGCCACT<br />
AAGTTTTATGGTGTTTTGTTCTGTAGCAGAAGCATAGGCATACTGACAATACAAACCGAAATCCTTCTAA<br />
CGTAGTGGACCTTTTCAGGCCAGCATTTTTTCCTTGAAAACCTGGAGCATGTATCCATCTTATAGCAGAG<br />
ATCACTTTCACAATGTTTGGGCTCTTGATTTGAATTGATGATGTAATGAGCCCTCTATCCAGATTGTAAC<br />
TAATTACTCTGCGAATTGACTGGATTCCACACCCTTCTAATATTTTACTTTTCCTCTTTTATCAACTCTC<br />
ATTCTTGCTGCCATGATCAATGGACCAACTATGCTTATAACCACAAATTTTGATATGCTTAAACAAATGA<br />
ACAAATATATTTAATAATTTCTTTTTTTTTTTTGAAATAGTATCTTGCTCTGTCACCCAGGCTGCAGTGC<br />
AGCAGCGTGATCTCAGCTCACTATAACCTCCACCTCCCGGGTTCAAGTGATTCTCCTGCCTCAGCCTCCC<br />
AAGTAGCTGGGACTACAGGCGCCCACCACCATACCTGGCTAATTTTTTGTATTTTTAGTAGAGACAGGGT<br />
TTATCCATGTTGGCCAGGCTGGTCTCAAACTCCTGACCTCAAGTGATCCTCCTGCCTCGGCCTCCCAAAG<br />
TGCTGGGATTACAGGTGTGAGCCACCATGCCCAGCCAATAATTTCCTGATATAATAAAAATGCCAATACT<br />
ATACAATTAAATAGTAAAGTGATAAAAAATAGGATAACATGATAACCACTAATTAATATATACTACATAA<br />
TCATC</dnaseq><br />
<br />
==Labs working on this lncRNA==<br />
* Institute of Biochemistry, Genetics and Microbiology, University of Regensburg, Regensburg, Germany.<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Yan X , Zhang D , Wu W , et al. Mesenchymal Stem Cells Promote Hepatocarcinogenesis via lncRNA-MUF Interaction with ANXA2 and miR-34a[J]. Cancer Research, 2017, 77(23):canres.1915.2017.<br />
</ref>(1)<br />
<ref name="ref2"><br />
Ziegler C, Graf J, Faderl S, et al. The long non‐coding RNA LINC00941 and SPRR5 are novel regulators of human epidermal homeostasis[J]. EMBO reports, 2019, 20(2).<br />
</ref>(2)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=LOXL1-AS1&diff=1276479LOXL1-AS12019-08-13T02:45:11Z<p>Qianpeng Li: </p>
<hr />
<div>==Annotated Information==<br />
===Name===<br />
Approved Symbol: LOXL1-AS1<br />
<br />
Approved Name: LOXL1 antisense RNA 1<br />
<br />
Chromosome: 15q24.1<br />
<br />
RefSeq ID: NR_040066<br />
<br />
OMIM ID: 616800<br />
<br />
Ensembl ID: ENSG00000261801<br />
<br />
Pubmed IDs: 26307087,30278884,29678575<br />
===Characteristics===<br />
[[File:LOXL1-AS2-exp-GBM.png|right|thumb|400px|LOXL1-AS1 expression and prognostic significance in CGGA datasets<ref name="ref1" />.]]<br />
===Function===<br />
* Silencing LncRNA LOXL1-AS1 was a new regulator of NF-kB signaling pathway through repressing RELB directly, resulting in increased marker genes of PN subtype and decreased those of MES. GBM cell proliferation was functionally suppressed by LOXL1-AS1's knockdown. Furthermore, RELB's rescue could reverse LOXL1-AS1's effects partially in GBM malignant behaviors<ref name="ref1" />.<br />
<br />
* LOXL1-AS1 regulates prostate cancer cell proliferation and cell cycle progression through miR-541-3p and CCND1<ref name="ref2" />.<br />
<br />
* LOXL1-AS1 plays a functional role in cellular stress response and correlates with the development of the exfoliation syndrome<ref name="ref3" />.<br />
<br />
* LOXL1-AS1 regulates the proliferation and metastasis of medulloblastoma by activating the PI3K/AKT pathway<ref name="ref4" />.<br />
<br />
===Regulation===<br />
<br />
===Diseases===<br />
Glioma<ref name="ref1" />. <br />
<br />
Prostate cancer<ref name="ref2" />. <br />
<br />
Exfoliation syndrome<ref name="ref3" />.<br />
<br />
Medulloblastoma<ref name="ref4" />.<br />
<br />
===Expression===<br />
LOXL1-AS1 is predominantly distributed in the cytoplasm<ref name="ref2" />.<br />
Compared with proneural, LncRNA LOXL1-AS1 expression is increased in mesenchymal<br />
subtype of glioblastoma<ref name="ref1" />.<br />
{| class='wikitable' style="text-align:center"<br />
|-<br />
! | Experiment<br />
! | Forward primer<br />
! | Reverse primer<br />
|-<br />
| rowspan="1"|Quantitative real-time PCR<br />
| | 5'-TTCCCATTTACCTGCCCGAAG- 3'<br />
| | 5'-GTCAGCAAACACATGGCAAC- 3'<ref name="ref1" /><br />
|}<br />
<br />
===Evolution===<br />
<br />
===Sequence===<br />
>gi|338827654|ref|NR_040066.1| Homo sapiens LOXL1 antisense RNA 1 (LOXL1-AS1), transcript variant 1, long non-coding RNA<br />
<dnaseq>GCACCGGCAGGTAGGGCGGCTCCAGCGCGCGCGGCGGCCCGTACGCCTCGGGCGGCGGGTTGGCGTAGGGCGGGTACCAGCCCAGGCGTGGGTCTCCGCCATGGGCCTGCGCCGCCTCGGGACCGGGGTCAGGGTGCCACGGCTTACCAATGGAAGATTAGGCCAGATGGCTCCTGAGAGTGCTTTGGGAGATTCTCTGTTCCTTCTGGGAATGGCAGGGATAGGAGGGGGTCCCAGAAGTTTGAACGCTTTGGCATCCAAGAAATCACACTCCAAATACTGCTCTTCTGGCCTCCCCTGGGCTGCCTTCTCCAACCGTGTTCCTGGGAACCGAAGGGCAGAAATTGCCCTCTTGGGCTTATAAACAAGGAGCTCCTGCCTGCCTGGATGAAGAGGAGGTCAAGACTTTGTCCCCCACTCCGCAAGATACCCTCTCTGTTCCGGAGCGGTGGGTCCCTCCCCTGTTAGGACCTTGTCTCCCTCAGGACTGGACCTGGATCCTGGGCCTGCAGTCAGATTGCCAGTTTCACTTAGAGGTGGAAATGTCAACCCACTGGTTGGAATGGGAAGGTGAGACAGGATTTCACCATGTTAGCCAGGATGGTCTTGATCTCCTGACCTCATGATCTGCCCACCTCGGCCTCCCAAAGTGCTGGGCTTACAGGCGTGAGCCACCGTGCCCGGCCAAAAATAACTTTTAAAAACATGAGTATAGCATACACACACACAAAAGTCCACAAATCCTAGGTGTACCACTTGATGAATGATCCCAACGTGAGCACACCTCTGGATTACCACCTGGATCAAGAAATAGGACATCACAGCAGCTGGCAGCTTCCAAGGAGAAGCTCTGGAAAGTTCTGCCTGTCTCAGCACCTGGCTGGATCGGAAACGAGTTTTCTTTAACCAGATTTTTAATGACTGACTTATGTGGACAAATCATAACTGAATGAATCACCTCCTTTGTTGATTTTTTTGGGTACTTTATTTGCTATTATAAATGATGCTGTAATAAGCACCCTTGAAGAAATCTTCATATCTGCCTCTCCTGTGTAGCAGGTCACAGTGCCTGGGTTTGGTTCTAGCCCTCATTTGTGAACTGTGTGACTCACCATGCCTTTTTTCTTTCTGTAAGACAGGAATAATGGTAAGAATTTAAATGGGGGTAATATGGAGCGCGTTTAGTTCAGAGCCTGGTGCATACAAGCACTCAATAAGTACTGGCGATTATTAGACCTTTAGATTAATTTATTAGAAGTTGGATTTCTGGTGAAAGGGTTTGAGTGTTTTTGAGGCTTTGGCACAGAATACCCAGCTGGTCCCAGAAAGGTGGTTCCCATTTACCTGCCCGAAGGTAATTCACCCTTACTGATACTGAGTACTGTTTTCTAAAAGAACATTAAAAATTGGATAGGTTAAAAACAGGTGAATACATTTTTTTAGTTGCATTTTTTTGGTTACCCGTGAGAGTGAACATGTTGCCATGTGTTTGCTGACCTCCTAAATGGTCTATTTGCTCCTACCTTTGTACCCCAAAAGTCTGCTCTCAAGATGGTAGCCAGAATGATCCTTTTTGAGACATAAGTCAAAATTTCACTCTTCTCCTTAAAGCTCTGCAATGGTTCTCAGGTTAAAAGCCAAAGTCCTGTTCAAGGCCTCCAGGGTCCTCACCACTTGGTCCCTTGCTCTTTCTGTTCTAGCCAACTTGGCCTTCTCCTGCCCCTCCGCCGCACCATGGCAATTTCCCCTGCTCTGTGTGGTCAACTACCTGAATCTGTTCAAAGCTTTGCTCAAATGTCTCCTTCCTGATGAGACCTCCCCAGCCCCTGAGCTCCCCATGCCTCACTCCTGATCGCCTTACTTAACCCTTCTTTTTCTTTTTTGCCAGTAGTACTTATCACCGTCTAAAATACTTCATAATTTACTTGTTTATTGTTTGCCCCTCTCCAATAGAATGTAAGCTCCTTGGGGCAGGGACCTTTGTCCTTTGTCTTGTTCACTGCTGTGTCCCATGTGTAAACTTGTCTGGCACAGAAGAGGTGCTCGATAAATATTTGTTGAGTGAATGAATGGTAAATTTTCTGTTCATATTCTTTGACTATTTTCTATTGTAATGTTCATCTTTTTAGTATTGGTTTATAAGATGTATATTTAGCACCTTTTCATATATCACTCTTTGTCACATATTATGCAACTAATTTGTCATTTCCATCAATTTTTAAAATACTTTCTTGATGCTTCATTTTTAAGCTGTCAGATTATTAATCTTTTCTTTATGGTCTTGGACTTTATTGTTGCATAACCGCTGCCTTCACCAGGAACATATAAATTTTCAATTAAATGTTCTTCTGAGATTTTATGATTTCACTTTTTATATTAAACTCTTCATTTTGTCTTCATGTGTGGTGAGAGGTAAGAACATAACTTTAAAGCAAATTAACCAACTATCCCCAAATGAATTATAAATAAATTAATCATTTTCCAATAAAAAAAAAAAAAAA</dnaseq><br />
<br />
==Labs working on this lncRNA==<br />
* Department of Neurology, The Second Affiliated Hospital of Dalian Medical University, 467 Zhong Shan Road, Dalian City, 116023, PR China<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Wang H , Li L , Yin L . Silencing LncRNA, LOXL1-AS1, attenuates mesenchymal characteristics of glioblastoma via NF-κB pathway[J]. Biochemical and Biophysical Research Communications, 2018:S0006291X18309148.<br />
</ref>(1)<br />
<ref name="ref2"><br />
Long B, Li N, Xu X X, et al. Long noncoding RNA LOXL1-AS1 regulates prostate cancer cell proliferation and cell cycle progression through miR-541-3p and CCND1[J]. Biochemical and Biophysical Research Communications, 2018.<br />
</ref>(2)<br />
<ref name="ref3"><br />
Genetic variants and cellular stressors associated with exfoliation syndrome modulate promoter activity of a lncRNA within the\r, LOXL1\r, locus[J]. Human Molecular Genetics, 2015, 24(22):6552-6563.<br />
</ref>(3)<br />
<ref name="ref4"><br />
Ran G , Rui Z , Cuicui Z , et al. LncRNA LOXL1-AS1 Promotes the Proliferation and Metastasis of Medulloblastoma by Activating the PI3K/AKT Pathway[J]. Analytical Cellular Pathology, 2018, 2018:1-11.<br />
</ref>(4)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=NONHSAT096369&diff=1276478NONHSAT0963692019-08-13T02:44:33Z<p>Qianpeng Li: </p>
<hr />
<div>''DANCR'': A valuable cancer related long non-coding RNA for human cancers<br />
<br />
==Annotated Information==<br />
===Name===<br />
Approved symbol: ''DANCR''<br />
<br />
Approved Name: ''DANCR'': Differentiation antagonizing non-protein coding RNA<br />
<br />
Alias names: "anti-differentiation ncRNA",<br />
"anti-differentiation noncoding RNA",<br />
lncRNA-ANCR<ref name="ref1" /><br />
KIAA0114,"KIAA0114"<ref name="ref2" /><br />
"small nucleolar RNA host gene 13 (non-protein coding)", SNHG13 "adipogenesis up-regulated transcript 2", ''AGU2''<ref name="ref3" /><br />
<br />
LncBook transcript ID: HSALNT0288925<br />
<br />
===Characteristics===<br />
The ''DANCR'' gene is 855-base-pair long noncoding RNA located on human chromosome 4, with the closest adjacent annotated genes located 54.8 kb upstream of (USP46) and 28.7 kb downstream from (ERVMER34-1) the ''DANCR'' locus. The ''DANCR'' locus consists of three exons and harbors a microRNA (MIR4449) and a snoRNA (SNORA26) in introns 1 and 2, respectively. These small RNAs are not coordinately expressed with ''DANCR'' and are not part of the mature ''DANCR'' transcript. <ref name="ref1" />.<br />
''DANCR'' contains another conserved GC-rich region in the first intron, which may be processed as a not-yet-annotated small functional RNA. This notion does, however, require more intensive analysis of the function of ''DANCR''. From an evolutionary perspective, it is of interest that transcription units of ''DANCR'' as well as AGD2 are shaped by retrotransposons. AGU2 contains a long terminal repeat (LTR)-like element, which provides its polyA signal.<ref name="ref3" /><br />
<br />
===Function===<br />
''DANCR'' suppresses a genetic program associated with epidermal differentiation. Depleting ''DANCR'' in progenitor-containing populations, without any other stimuli, led to rapid differentiation gene induction. In epidermis, ANCR loss abolished the normal exclusion of differentiation from the progenitor-containing compartment. The ''DANCR'' lncRNA is thus required to enforce the undifferentiated cell state within epidermis <ref name="ref1" />.<br />
<br />
===Regulation===<br />
''AGU2'' induction conteol ''DANCR'' regulation<ref name="ref3" />.<br />
<br />
===Disease===<br />
*Breast Cancer <ref name="ref4" /><br />
*Colorectal Cancer <ref name="ref4" /><br />
*Hepatocellular Cancer <ref name="ref4" /><br />
*Gastric Cancer <ref name="ref4" /><br />
*Glioma <ref name="ref4" /><br />
*Osteosarcoma <ref name="ref4" /><br />
*Prostate Cancer <ref name="ref4" /><br />
<br />
===Expression===<br />
Long non-coding RNAs-''DANCR'' is a valuable cancer-related lncRNA that its dysregulated expression was found in a variety of malignancies, including hepatocellular carcinoma, breast cancer, glioma, colorectal cancer, gastric cancer, and lung cancer. The aberrant expressions of ''DANCR'' have been shown to contribute to proliferation, migration, and invasion of cancer cells <ref name="ref4" /><br />
===Sequence===<br />
>gi|57291|ref|024031.2|Homo sapiens differentiation antagonizing non-protein coding RNA (DANCR), transcript variant 1, long non-coding RNA<br />
<dnaseq>CCTCGCGACCCTCCTGCTTCCCTCCCCGCCCCGCGCCGCCTCTCTGGTTTGTGCGCCCGTCGCAGGTCGCAGGCCTCTTTGTCAGCTGGAGTTGCGCGGGCTGACGCGCCACTATGTAGCGGGTTTCGGGCGGGCCACGCGTGCGGGACAGGAACCCAACCCCAGCCGACCTTGAGCTCCAGGAGTTCGTCTCTTACGTCTGCGGAAGTGCAGCTGCCTCAGTTCTTAGCGCAGGTTGACAACTACAGGCACAAGCCATTGAAGCTGGAATGTCCTGTTGCTGGTATTTCAATTGACTTAAGCCAACTATCCCTTCAGTTACAATAGGAAAGTGCCTCTAATAAGGCCAAATATGCGTACTAACTTGTAGCAACCACGTGTCCGTGCAGTGCCACAGGAGCTAGAGCAGTGACAATGCTGGTGGCAACAGGGCAGTGTAGCAGGTGCTTCATGTTCACCTTTTCAACCTTTTCATTTAATTGTCACAACTCGGAGGTGGATTCTGTTAGGGACAGGCTGCCCCAGGACCACTCCGCCCCCGCTAACTCAATGCAGCTGACCCTTACCCTGAATACTCTGCAGCTGCATTCCTGAACCGTTATCTAGGCGCTATAGCAAGGTCACCAGACTTGCTACACCGAAGCCCTCTGGGTGGCACGGGGGAGGTCATGAGAAACGTGGATTACACCCCCTTGTAAATTCCTATTTTCACAAGATAATATATTGTAAGCCGGTCATGAGATTATATGTGGTAAAGTTAATTGACTAACAACCCCAGGGTCTCTCTCCCCCATATAAACCCCTCATTTTGTAAGCTCAGGGCTGCCACCTCCGACTGGTGGAGAAGCCTGGCAGGTTAATAAACTTACTTGGCCTGA</dnaseq><br />
==Labs working on this lncRNA==<br />
*Veterans Affairs Palo Alto Healthcare System, Palo Alto, California 94304, USA.<br />
*Kazusa DNA Research Institute, Chiba, Japan<br />
*Department & Program of Clinical Laboratory Medicine, Center for Gene Diagnosis, Zhongnan Hospital of Wuhan University, Wuhan China<br />
*Department of Pain Management, Zhongnan Hospital of Wuhan University, Wuhan 430071, China<br />
*Department of Radiology & Nuclear Medicine, Zhongnan Hospital of Wuhan University, Wuchang, Hubei Province, Wuhan, 430071, China<br />
<br />
==References==<br />
<references><br />
<ref name="ref1">Kretz M, Webster DE, Flockhart RJ, Lee CS, Zehnder A, Lopez-Pajares V, et al. Suppression of progenitor differentiation requires the long noncoding RNA ANCR[J]. Genes & development. 2012,26(4):338-43.</ref>(1)<br />
<ref name="ref2">Nagase T, Miyajima N, Tanaka A, Sazuka T, Seki N, Sato S, et al. Prediction of the coding sequences of unidentified human genes. III. The coding sequences of 40 new genes (KIAA0081-KIAA0120) deduced by analysis of cDNA clones from human cell line KG-1[J]. DNA research : an international journal for rapid publication of reports on genes and genomes. 1995,2(1):37-43.</ref>(2)<br />
<ref name="ref3">Kikuchi K, Fukuda M, Ito T, Inoue M, Yokoi T, Chiku S, et al. Transcripts of unknown function in multiple-signaling pathways involved in human stem cell differentiation[J]. Nucleic acids research. 2009,37(15):4987-5000</ref>(3)<br />
<ref name="ref4">Thin KZ, Liu X, Feng X, Raveendran S & Tu JC. LncRNA-DANCR: A valuable cancer related long non-coding RNA for human cancers[J]. Pathology-Research and Practice. 2018<br />
</ref>(4)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=DGCR5&diff=1276477DGCR52019-08-13T02:40:55Z<p>Qianpeng Li: </p>
<hr />
<div>''DGCR5'', is a long noncoding RNA involved in DiGeorge syndrome<br />
<br />
==Annotated Information==<br />
===Approved Symbol===<br />
''DGCR5''<br />
===Apprroved Name===<br />
''DGCR5'': (DiGeorge syndrome critical region gene 5 (non-protein coding))<br />
NCRNA00037, LINC00037 <ref name="ref3" /><br />
<br />
===Characteristics===<br />
In humans, ''DGCR5'' is located on chromosome 22q11, at the ADU breakpoint <ref name="ref4" />.<br />
''DGCR5'' originates from a cis-acting transcriptional control element in the vicinity of the ADU/VDU breakpoint.<ref name="ref1" /><br />
<br />
===Function===<br />
''DGCR5'' is a functional RNA; production of ''DGCR5'' transcripts is necessary for regional transcriptional control.<ref name="ref1" /><br />
Production of ''DGCR5'' transcripts is necessary for regional transcriptional control and ''DGCR5'' transcripts are merely a reflection of a particular chromatin configuration maintained over the region encoding the gene.<ref name="ref1" />.<br />
<br />
Long non-coding RNA ''DGCR5'' is involved in the regulation of proliferation, migration and invasion of lung cancer by targeting miR-1180 <ref name="ref7" />.<br />
<br />
''DGCR5'' promotes the lung adenocarcinoma (LUAD) progression via playing anti-apoptosis roles. Mechanically, it exerts its biological functions through regulating miRNA miR-22-3p in a ceRNA manner<ref name="ref8" />.<br />
<br />
===Regulation===<br />
Expression of ''DGCR5'' is regulated by the transcription factor REST. <ref name="ref2" /><br />
<br />
===Disease===<br />
*Clear cell renal cell carcinoma <ref name="ref1" /><br />
*Digeorge syndrome <ref name="ref1" /><br />
*Clear cell renal cell carcinoma <ref name="ref5" /><br />
*Lung cancer susceptibility <ref name="ref7" /><br />
*Velocardiofacial syndrome <ref name="ref6" /><br />
*Lung adenocarcinoma (LUAD)<ref name="ref8" /><br />
<br />
===Expression===<br />
''DGCR5'' inhibited the expression of AKT, GSK-3β, and β-catenin by targeting miR-1180 <ref name="ref7" /><br />
''DGCR5'' is expressed during human and murine embryogenesis <ref name="ref1" /><br />
<br />
''DGCR5'' was upregulated in LUAD tissues and LUAD cell lines. Inhibition of ''DGCR5'' can prevent LUAD progression via playing anti-apoptosis roles. Both mRNA expression and protein levels of BCL-2 were increased by DGCR5 downregulation while reversely BAX was increased<ref name="ref8" /><br />
{| class='wikitable' style="text-align:center"<br />
|-<br />
! | Experiment<br />
! | Forward primer<br />
! | Reverse primer<br />
|-<br />
| rowspan="1"|Quantitative real-time PCR<br />
| | 5'-CACGAGTGTAGTGCCCAGTT- 3'<br />
| | 5'-GGTCAGGGACCTTTGTCGTT- 3'<ref name="ref8" /><br />
|}<br />
<br />
===Sequence===<br />
>gi|345842381|ref|NR_002733.2| Homo sapiens DiGeorge syndrome critical region gene 5 (non-protein coding) (DGCR5), transcript variant 1, non-coding RNA<br />
<dnaseq>GCGCGGAGCCTAGACCCGCTGCCGGGCCGGGGCTGGGCCGGAGCGGCGGCGCCTGGATGCCGGCCCGGGGCTGGGCCGGAGACTGGCGCCCGCCCCGAAGCGACTTTCGGTCCCCGACCCGCTCCGCCTGACCCCTATGATGAAGAGGGCGTCCACTGGAGTTCTTGCTGTCGACATCTTTGACAAGTTCAACTTCACGGGAGCCAGAGTCCCATGGTTCGACGCCATTCATGAAGAATTCCCCAGGGAGCTGGAGTCCTCCATCTCCTTCCCAGCCAACTTCTTCAAACCACCTGAAGAAAAAGAAGGCCCCCTGGTAAGGCCAGCCAGCCGGAGGACCACCCCGCAGACCACACGCCCAGGGCCTGGCACCGAGGGGGAGGCCCCGATCAGCAGGTGAAAGCGACACCCTGATGACACTGGCTAGTTCACCTTCACTCTGGTCATCGTTTACTGTACCCCGGGGCAGCTCCCGCCTGAGCCCTATGACCCCAACCGCCGCAGCCTCTGGCTGCCTCACTGGCCCATCATTAATACGTCGATGGTGAGCGCACTGGTGTACAGCGAGGGGGCTCCACTTCCGAGACCCCTGGAGAGGCCCGTCCTGGTGGAGTTCACCCTGCTGGAGATGGAGAAGCGAACCAAGCCTGTCTGTGTGTTCTGGAACCATTCCCTGGCGTAAATGTGATGCCGGGAGTTCTGCATCTTCATGTGAGGGCTTTGCCAAGACACAGAGAACCCGCAGGGTTGTTGGCTCAGCGGCAGATCGTCCCACGGGGACAGTCTCTTGTGGTCTGTGTCTCCCCCTTCAGCCCCCTGTGGGGCAGTGAGCCTCCTGCTCTGCTTCTGTGGGTGCATCAGAGCCCCCCCAGATGCCCACACGCAGACGCGCACAGGCCTGCACGTGGAAACACAGACATGCGCACACGCAGGCCCACACACAGACGCACACAGAGCTGCACGTGGAGACACGTGCGCACACGCAGGCCCACACGCAGGCCCACACACAGGTGCACGCGGACCTGCACGTGGAGACACAGATGTGTGCACATGCAGGCCCACACACAGGTGAGCGTGGACCTGTGTGAACAGATGCGCGCAGACCTGCACGTGGAGACACAGACATGCAGGCGCACAAAGAGATCCCTCAAGGCTGACACCCAGGAAGGGGCCTCTCACTTGTGGGACTCCCGAGATGCAGTGGCCAACACGAGTGTAGTGCCCAGTTCACTGCTGGATAAGACAGAGGCCTGTTCTGGTCACACATGGGAGGCAGAACCCAGAGACTGGGCCCAGGAGCCCTTCTGCTGACAGTGGGAACTCCCAGCTACGTGTGGGGGTCCCCATACCAGACAAAGGTCCCTGACCTTAGTCTTGCCCGAGAGGCCGACACAGCCCAGCTTTGGGGTCTGGCTTTACCCACAAGAGGCCACACCTTGCCACAGCACTGTTTATCTGGCCTGTTTCAGAAGCACCGTCAGAGTGGCGAAGGCAGGAGGTGGTGCACGAGAGTCTACGTTCTAGCATCCATTCAAGTGAGGGAAAGGCGTTTCGTACTTAGAAAAATGCAAAATTAATGATTCTCACCCACACATGAGACTGTGGATTCACCCATGTATGAGATAGTGGATTCAGAGCCATGCTGTGGCTCTCATCTGCTGGGAGCCAGTAGTGTTTGTGCTTTGGTTTTGCTTTTTTAGCTACATGGTTTATGTGAGGTGCGGACTTACTTGAGTTGCTCTGTCTTTACAGGGAGCTTGCTTTTTCTCTGCTGGTTTGTTTTCACTTTTGCTGTCTCTGTTTAGAAGAAAACATTAGAACTGGGGTGTGGTGGAAGGATGGGAGCACAATCTGGGAGGGGAAGACCTGCTCTCTCTCCACATACCAGGAGGGAGTGGCAGGAAGGGGAGACACTGTGCCGGACTCAGGGAGTCAAGAGCGTGAGCACCCCCAGGCTTCAATCTGCTGAACGTTGTGCATCTGGGGGCGCCCGTGCAGCAGGAACACTCTCCCCATCACAATTCCTCTGGGCACAGTGGAGAGCCATGAGTGGGGGCTGTCCTGGGGGCTGCGCTATGGTGAGTGAGCCCACGCCAGGAGCCAGTTCAGCCCAGCCTCATTCTTCTCCTGCTTCTTTGCTTTCCAAGTTCTAGTTCATAAGCAACCAGCACAGTACCTGGAATGTAAGAGGCGCTTGGCTTATAAAAGAGAGAAGAAAGGAACCCCTTTCACCACGAGGGACGTCAGGCCCAGCTCTCTGTCCCGGGCATTCATCTTTTTTCCGGCAATTAGCTTCAGCTCTAATGACCTGCTGTCTGCTTTATGTTGCACCTATGATTTCCAGATTGTAAAGTTTGTGGCAAATGTATTAACGTTCACATCCCATTTACAGATTAGCAAACTAAGGATCTGAGAGGTTATGTGATTTTCCCAGTCTGGCGGAGGGCAGGGCCCTGTCAGAAGCCGAGACACACCTCGTAACAGCTTGTTATTTGGGGCTTCCCATCAGTGAGGCAGGAGTCATAATGGGGCCCTGGCTTCTGGGCAATTCCCATAAAACATTGTGCCACCTGAAGATGGAAGTGTCAGAGGAAGGCGAGATGTTATTTCTGAAAGCATCTACCCTCAGAAAGAGACAGAGGAGTGCATCGCAGCTGTGTGAACCCGGGGTGGTGGTGGTTCCAGCAGCGGGGCACGTGGTGGACGCAAGACGGCCCCGTTTGAGTTTTGCTGCTAGGTGACATGTAGAACTTGAACTTCAGAGGGTGCTCCTTGGAGGCCCTGATGAGAGAGACACAGAAGGGAAGGGAGACTGTTCCCATGGTCCTGCCTCTGCGGCAGCGAGCCTGCTGCTCTTGCAGCTGGGTGGCTGTTCGGTGCAGGGGGCCGGTGAGGAACACGGTGGGGAGCAGCCTGCGAGGGCGCCGGGCTTTCAGCACTCACTATACCTGCTGTTTGGTTTGGCCAGGATGGCCTGGGAGTCCCCAGGGCCGGGCAAAGACTGCCCCCAACAGACATGGGCGGAGGGAACCGTCTCACCCCTGCCTCTTCTCCCTTCTCTACGCAGTGTCAGTGGGACGGGAGGGTGGTCTGCCCGGGGCTTCAAGCTCCTGTCCAGGAACCGGACCCATGTCGTACGCCAGTGCAGCCACACGGCCAGCTTCGAGGTGCTCATGGACGTCTCCAGGTGTGAGATGGGCATCTTCTTGTGGCCACTATGCCCGCTGAGCCTACCCCCAAACCTGCCCCTCCTCAAACTAAATCTTCCATTCTAAGCGCTTTGAACGAAGCAAATCAACCAATTAAAAAAATATATTCCAGGAAAAAAAAAAAA</dnaseq><br />
<br />
==Labs working on this lncRNA==<br />
*Molecular Medicine Unit, Institute of Child Health, London<br />
*Department of Pulmonary Medicine, Sir Run Run Shaw Hospital of Zhejiang University, Hangzhou 310016, Zhejiang Province, China,<br />
*Department of Hepatobiliary and Pancreatic Surgery, Huai’an First People’s Hospital, Nanjing Medical University, Huai'an, Jiangsu 223300, People’s Republic of China<br />
*Molecular Medicine Unit, Institute of Child Health, London<br />
<br />
==References==<br />
<references><br />
<ref name="ref1"> Sutherland HF, Wadey R, McKie JM, Taylor C, Atif U, Johnstone KA, Halford S, Kim UJ, Goodship J, Baldini A,Scambler PJ. Identification of a novel transcript disrupted by a balanced translocation associated with DiGeorge syndrome. Am J HumGenet. 1996 Jul;59(1):23-31. <br />
</ref>(1)<br />
<ref name="ref2"> Johnson R, Teh CH-L, Jia H, Vanisri RR, Pandey T, Lu Z-H et al. Regulation of neural macroRNAs by the transcriptional repressor REST[J]. Rna. 2009, 15(1):85-96.<br />
</ref>(2)<br />
<ref name="ref3"> Huang R, Wang X, Zhang W, et al. Down-regulation of LncRNA DGCR5 correlates with poor prognosis in hepatocellular carcinoma[J]. Cellular Physiology and Biochemistry, 2016, 40(3-4): 707-715.<br />
</ref>(3)<br />
<ref name="ref4"> Sutherland HF, Wadey R, McKie JM, Taylor C, Atif U, Johnstone KA, Halford S, Kim UJ, Goodship J, Baldini A, Scambler PJ (Jul 1996). "Identification of a novel transcript disrupted by a balanced translocation associated with DiGeorge syndrome". American Journal of Human Genetics. 59 (1): 23–31. <br />
</ref>(4)<br />
<ref name="ref5"> Yu G, Yao W, Wang J, et al. LncRNAs expression signatures of renal clear cell carcinoma revealed by microarray[J]. PloS one, 2012, 7(8): e42377.<br />
</ref>(5)<br />
<ref name="ref6"> Qureshi IA, Mattick JS & Mehler MF. Long non-coding RNAs in nervous system function and disease[J]. Brain Res. 2010.<br />
</ref>(6)<br />
<ref name="ref7"> Chen EG, Zhang JS, Xu S, Zhu XJ & Hu HH. Long non-coding RNA DGCR5 is involved in the regulation of proliferation, migration and invasion of lung cancer by targeting miR-1180[J]. Am J Cancer Res. 2017<br />
</ref>(7)<br />
<ref name="ref8"><br />
Dong H X , Wang R , Zeng J , et al. LncRNA DGCR5 promotes lung adenocarcinoma (LUAD) progression via inhibiting hsa-mir-22-3p[J]. Journal of Cellular Physiology, 2017, 233(29).<br />
</ref>(8)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=DGCR9&diff=1276476DGCR92019-08-13T02:39:56Z<p>Qianpeng Li: </p>
<hr />
<div>==Annotated Information==<br />
===Name===<br />
Approved Symbol: DGCR9<br />
<br />
Approved Name: DiGeorge syndrome critical region gene 9 (non-protein coding)<br />
<br />
Synonyms: DGS-A, POM121L5P<br />
<br />
Chromosome: 22q11.21<br />
<br />
RefSeq ID: NR_024159<br />
<br />
Ensembl ID: ENSG00000273032<br />
<br />
LncBook transcript ID: HSALNT0275220<br />
===Characteristics===<br />
<br />
===Function===<br />
* DGCR9 was positively associated with lymph node invasion and tumor-node-metastasis (TNM) stage in gastric cancer patients. By in vitro functional analysis, knockdown of DGCR9 in gastric cancer cells suppressed cellular proliferation, migration, and glucose uptake. In contrast, overexpression of DGCR9 increased each of these cancer cell characteristics<ref name="ref1" />.<br />
===Regulation===<br />
<br />
===Diseases===<br />
Gastric cancer<ref name="ref1" />. <br />
<br />
===Expression===<br />
DGCR9 was significantly upregulated in gastric cancer tissues and cell lines<ref name="ref1" />.<br />
{| class='wikitable' style="text-align:center"<br />
|-<br />
! | Experiment<br />
! | Forward primer<br />
! | Reverse primer<br />
|-<br />
| rowspan="1"|Quantitative real-time PCR<br />
| | 5'-TAGCATGGCCAGGTATGCAC- 3'<br />
| | 5'-TGCGAATCCCAAAGCTGTCA- 3'<ref name="ref1" /><br />
|} <br />
<br />
===Evolution===<br />
<br />
===Sequence===<br />
>gi|205830460|ref|NR_024159.1| Homo sapiens DiGeorge syndrome critical region gene 9 (non-protein coding) (DGCR9), long non-coding RNA<br />
<dnaseq>GTAAAACTCATATGAAACCAAAAAAGAGCTCAAAGAGCCAAAGTCATCCTCAGCAAAAACAACAAAACTAGAAGCACCCCATTTCACTGCAAATTAGAATGACAAAATTTTTGACAAGTGCATGGTAACCAAAACAGCATGGTCCTAGCATAAAACTAGACACATAGATCAATGGGACGGATGACAGAGCCCAGAAAGACAGCCACATAGTCTTGGGGCTTGTGTCTCTCCTGCTGTGCATCCATGCTGGGTGCTTTACATACAACAGGCAGACAAGAAGTCCCTGTTGCAAGTGAGGACAAAGTGTGGGAAGGCCGTGAGGGTCTGCAGTCCCAGATGGCCTTGGCCTCACCCCGCAGTGCGCTTTTGCACCAGAGTGCCACCTTCTTCTCCAGGTCCAGGTCTTCAGCAGTGACCCCAGACCCCAGCTGTAAGGGAGGTGGCAGCATCAGAGGCTCCCCTTGCCTGAGTGGCAGCAGAGGAAACTTGCATCTATGGGGCCTAGAGGCCTGGGATGTGGGGGAGCCATTCCTGGGGGCAAGTGTCTGCCCTGGTGCTGCATCTGCTGCCTTTTCACACTGGGTGAGACCCCAAGAGACAGCCTGAGGCCGGTCCTCACTCACTGTCTTTGAGGACCTGAGGGGCAGCTGACAGTGGGATGAGGCTGGCCCCCTCCTCTTTGGTGACAGGAAGCCTCCCATGGAACTGTAGGAGCTCACGATGGCATTTTGTTTGGTGCACGAACTCATCCAGGAGGTCTGGGATCTCTGGTTTTATCCGACTTCTGACCTCTGGGCATGGAGGTCTCTCTGCAGAGGCCCAGGCCTGGGCACGAAGGGAGAGAGGCCTCCATTGTCCCACAGGGGCCTAAATGCAGACTGTGCATCCCCGGTGCCCTCAGGAACCCTTCTCTGATCATCAGGATTCTCTTGGACTCTGGGGTCCTTGTCCTGCTCAGGCATCCCTGCCCCCCTCTTCAGGAGGGCCCTCAACACGATCTTCTCTGGACAGGAGTCTGGGGCACAACTGGATGTTGTGGGCCCCAAAGGGGTGACTCCCTGCTCCTGGGCCCCACAGAGAGTCCTTGTGCTCAGTGCACTGGCTGAGCTGCAAGACATCCTGGAATTGGGAGCACACAGCACCGGCTTGCTGTGGTACCTGTGCATTCAAATTGAAGGCAGGATCGCCAGCAAGGAACACAGGGCTTGCAGGATCACAGAAAACCCTTGGAGTTGTTTTGACACACCACTGATGCCAAGTGTCTGGGTACTTGTAGGATGGCCCTGCCATTCCATCCAGGGGCAGTGGCAACAGGGAGATTCCACAAACAAAGTGAACTGGGGGATGGGATGAGCAGGCTCCAGGCAACTGAGCCCTACTGGCAGGCCCTTGGCCCCCGGGGCCGGGACAGGGGTGACAGACACAGAGTGCCCAGGTAACCACTCCTGGGAGCAGTGGGGAACCGTCGGATGCTTCAACTCTTGAGAGCTGGGCTCTAAGCATCCGCCTTAGCTGCCAACTTGGCCAAAGGCTATGCGAGCAGTTTCCCGTTGACGGGCAATGCATCTTTCCAACCTGAGCGAGTGGGTGTGTGTGCAAAGATGGTGCGAGTCACGGATCTGCGCAGGAAGGGTGACTTTAAGGGATTAGCATGGCCAGGTATGCACACAAGGCACCTGCTGGCAATGCCTTGGTGGGGAGCGGGCAGTGCACACAAGAGGTACTGGAGGGAGAGGCGCGCGGGAAGAACAGGCGCGCACAATGGCTGCAGATCCACCTGTGGATCGCTGAAGATTCCTGCTGAGGGTTGAGGCTGCTGGGCTGGAGGACTGTATGGTCCATGCATTGTAATGTCCCCTTCTCTCCCTGGCCCGGAGCCCCAAGAGCTATCCGGACTCTCTCCAAGACCTGGTTCTGGCCCAGCAAAGAGGTCTCGGCAGGGGAGCAGGATTCCCGGCCCAGCAGCTGGCTCAGGAGGTGACAGCTTTGGGATTCGCATCTGAGCATCCTCCTACTCTTCTCCTGGGAACTCTGTTGGGGAGGGTTGCTCAGAACAGAAGTGCCTGGGACGCCCAGATCCTGCTGGAGTGGCAGCTGGGGTGATGGCCAGGGCAGGCTGGGAGGGACATACTTTCCATAGGACCCAGTGCTTTCATCTCCGTGCAACTGACCAAGAGAAACCAAACCCAAACTCCTTCCTTTACACAGACCTATTTGAGGGAGGCTGGGTATTGTTTGTGTATTTCAACCTAACAAGATTTTGAGATAGTTGGAATGCAGAAGGAGACAGGAGGACTCAAGTGTCCTGTCTTTTGCAAAAATGTCAAACGTAGCTACTCAGTCTCTTTTTTGTTTTTTTGTTTGTTTTGAAGACTATGGTTATTTTGCAAAATATATATTATTTGAGTTTCTCTAAAAAAAAAAAAAAAAAAAA</dnaseq><br />
==Labs working on this lncRNA==<br />
* Department of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo, People’s Republic of China.<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Ni C, Yang P, Guo J, Ye M. Role of DiGeorge syndrome critical region gene 9, a long noncoding RNA, in gastric cancer. Onco Targets Ther. 2018 Apr 19;11:2259-2267. <br />
</ref>(1)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=TP53TG1&diff=1276475TP53TG12019-08-13T01:56:59Z<p>Qianpeng Li: </p>
<hr />
<div>''TP53TG1'', a p53-induced lncRNA, plays a vital role in the progression of human cancers.<br />
==Annotated Information==<br />
Approved Symbol: ''TP53TG1''<br />
<br />
Approved Name: TP53 target 1 (non-protein coding)<br />
<br />
Previous Symbols: TP53AP1<br />
<br />
Synonyms: H_RG012D21.9, LINC00096<br />
<br />
Chromosome:7q21.1<br />
<br />
RefSeq ID:NR_015381<br />
<br />
OMIM ID:616403<br />
<br />
Ensembl ID: ENSG00000182165<br />
<br />
LncBook ID: HSALNT0289272<br />
===Characteristics===<br />
''TP53TG1'' , a long intergenic non-protein-coding RNA with 751 nt in length, was revealed to exert a tumor-suppressor feature in human cancer <ref name="ref1" />.<br />
===Function===<br />
[[File:TP53TG1exp.png|right|thumb|400px|TP53TG1 expression levels in NSCLC tissues and cells.<ref name="ref3" />.]]<br />
* It is reported that ''TP53TG1'' under glucose deprivation might facilitate cell proliferation and migration by affecting the expression of glucose metabolism related genes in glioma<ref name="ref2" />.<br />
<br />
* ''TP53TG1'' increased the sensitivity of NSCLC cells to cisplatin by modulating miR-18a/PTEN axis, elucidating a novel approach to boost the effectiveness of chemotherapy for non-small cell lung cancer (NSCLC)<ref name="ref3" />.<br />
<br />
===Regulation===<br />
<br />
===Diseases===<br />
Glioma<ref name="ref2" />.<br />
<br />
Non-small cell lung cancer<ref name="ref3" />. <br />
<br />
===Expression===<br />
''TP53TG1'' level was downregulated in cell lung cancer (NSCLC) tissues and cell lines<ref name="ref3" />.<br />
<br />
{| class='wikitable' style="text-align:center"<br />
|-<br />
! | Experiment<br />
! | Sense primer<br />
! | Antisense primer<br />
|-<br />
| rowspan="1"|Quantitative real-time PCR<br />
| | 5'-ACGAAGGTACCCAACCCTCT- 3'<br />
| | 5'-GGTGTAAGTGTTCGCCTGGT- 3'<ref name="ref3" /><br />
|}<br />
<br />
===Evolution===<br />
===Sequence===<br />
>gi|168823573|ref|NR_015381.1| Homo sapiens TP53 target 1 (non-protein coding) (TP53TG1), long non-coding RNA<br />
<dnaseq>CCCTGTCTCCAGTGGGCGTCTTGGGCCCCGGCTCTATTCTGGGCTGCGGGCCTGGGAAGGGCTCGCCGGGTGCCAAATGAGCTGTCCTAACTCTGCGGGGCTGCAGCTTCCTGCATGATGCTGGGGAGCTTGGCGCCTGACCCAGGATCTAGAAGGCACTCTGGGCAGGCCGCGCTCCGCCCACGAAGGTACCCAACCCTCTGGGATAGATGCAGGAAGCGATGGTTAAGACCCATTTTCACCCAACTTCTCGCCGCAGGTCTGGCTTACCACACGCTCCTCCCCATTCCCAGTGAGCCGCTTTTTGCAGCACCAGGCGAACACTTACACCAGTGCTTTGTAAAGGAATCTTATTGTCCACCCCGTGTCTTGGCAAAAGAACAGTGATCACACAGATTCCTACTTGGGCTCTTTCCTTTAATCTTCGGAGGCTGAGTTTGCCCAACTCAGGTTTAACCACCAAGGACTCTGAGAGCTGGCAGGTCTGAGTAACCCTGGTAACAATTCTCTTCACCTTATCAAAACCTGAGCTAAAACCAATGCATCAGCTGATGATGACAGCAGAGAGTGGCAGGGCTGAGGACCCAAAGTCATTTCCCAGGCTGGCGGAGAATAAACTGCCAGGGAGAAGAATGAGAAGACAGGAGACAAACTGTTTGGAAAGCTAAATCTTCCCTCTTAATGAATAAAGGTTTTTGCCTTGTCTTAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAA</dnaseq><br />
<br />
==Labs working on this lncRNA==<br />
* Department of Radiology, The First Affiliated Hospital of Zhengzhou University, No. 1 Jianshe East Road, Zhengzhou 450052, China.<br />
==References==<br />
<references><br />
<ref name="ref1"> Diaz-Lagares A, Crujeiras AB, Lopez-Serra P, Soler M, Setien F, Goyal A, et al. Epigenetic inactivation of the p53-induced long noncoding RNA TP53.<br />
</ref>(1)<br />
<ref name="ref2"> Chen X, Gao Y, Li D, Hao B, Cao Y. LncRNA-TP53TG1 participated in the stress response under glucose deprivation in glioma. J Cell Biochem.<br />
2017;118(12):4897–904<br />
</ref>(2)<br />
<ref name="ref3"> Xiao H, Liu Y, Liang P, Wang B, Tan H, Zhang Y, Gao X, Gao J. TP53TG1 enhances cisplatin sensitivity of non-small cell lung cancer cells through regulating miR-18a/PTEN axis. Cell Biosci. 2018 Mar 22;8:23.<br />
</ref>(3)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=NONHSAT007663&diff=1276474NONHSAT0076632019-08-13T01:55:12Z<p>Qianpeng Li: </p>
<hr />
<div>''GAS5'', functions as a ceRNA to regulate hZIP1<br />
<br />
==Annotated Information==<br />
===Name===<br />
Approved symbol: ''GAS5''<br />
<br />
Approved name: ''GAS5'': growth arrest specific 5<br />
<br />
Alias symbols: SNHG2, NCRNA00030<br />
<br />
HGNC ID: HGNC: 16355<br />
<br />
LncBook ID: HSALNT0017702<br />
<br />
Ensembl ID: ENSG00000234741<br />
<br />
RefSeq ID: NR_002578<br />
===Characteristics===<br />
''GAS5'' the Growth arrest-specific transcript , multiple splice isoforms of ~250, ~450, ~600nuc and longer, encodes 9 (10 in humans) snoRNAs in its introns. <ref name="ref1" /><ref name="ref2" /><ref name="ref3" /><ref name="ref4" /><br />
<br />
''GAS5'' is one of the lncRNAs in a six-lncRNA signature that is independently associated with the prognosis of GBM patients<ref name="ref9"/>. <br />
<br />
===Function===<br />
''GAS5'' is necessary and sufficient for growth arrest in human peripheral blood T-cells. It functions by controlling apoptosis and the cell cycle in lymphocytes <ref name="ref3" />. <br />
In some cell lines certain ''GAS5'' isoforms act to sensitise the cells to apoptosis but can't induce apoptosis on their own. In other cells types Gas5 can both induce apoptosis and growth arrest and sensitise the cells to further apoptosis <ref name="ref5" />.<br />
''GAS5'' carries out its function by binding the DNA binding domain of the glucocorticoid receptor (GR) with a sequence that mimmics the glucocorticoid response element (GRE). ''GAS5'' is translocated into the nucleus bound to the GR where it prevents GR from binding GREs and regulating transcription of target genes including apoptosis inhibitors <ref name="ref7" />.<br />
''GAS5'' also appears to repress the action of many steroid hormone receptors, showing some similarities to another lncRNA SRA <ref name="ref7" />.<br />
''GAS5'' is a snoRNA host and a functional RNA. Function does not require putative but nonconserved ORF, or the intronic snoRNAs <ref name="ref5" /><ref name="ref6" /><ref name="ref7" />.<br />
<br />
===Regulation===<br />
''GAS5'' can be regulated by mTOR, with mTOR (which promotes cellular proliferation) acting to inhibit the function of ''GAS5'' <ref name="ref6" />.<br />
Expression of ''GAS5'' mRNA is regulated at the posttranscriptional level during growth and at the transcriptional level in<br />
differentiated cells <ref name="ref2" />.<br />
<br />
===Disease===<br />
*Autoimmune disease <ref name="ref6" /><br />
*B-cell neoplasms <ref name="ref6" /><br />
*Breast cancer <ref name="ref5" /><br />
*Kidney cancer <ref name="ref6" /><br />
*Lymphoma <ref name="ref6" /><br />
*Prostate cancer melanoma <ref name="ref6" /><br />
*Systemic lupus erythaematosus <ref name="ref6" /><br />
<br />
===Expression===<br />
''GAS5'' is widely expressed in adult tissues and over embryonic development <ref name="ref1" />. Transcript undergoes post-transcriptional regulation, highly unstable but stabilised by growth arrest, serum starvation and inhibition of protein synthesis <ref name="ref2" /><ref name="ref4" /><ref name="ref7" />. Associates with ribosomes in the cytoplasm <ref name="ref4" />. Localises to both the nucleus and the cytoplasm <ref name="ref7" />. Down-regulated in breast cancer <ref name="ref5" />. Transcript was classified as unstable with a half-life >4 hr in human Hela cells <ref name="ref8" />. <br />
===Sequence===<br />
>gi|60674|ref|NR_002578.3| Homo sapiens growth arrest specific 5 (GAS5), transcript variant 1, long non-coding RNA<br />
<dnaseq>GTCTTTTCGAGGTAGGAGTCGACTCCTGTGAGGTATGGTGCTGGGTGCAGATGCAGTGTGGCTCTGGATA<br />
GCACCTTATGGACAGTTGTGTCCCCAAGGAAGGATGAGAATAGCTACTGAAGTCCTAAAGAGCAAGCCTA<br />
ACTCAAGCCATTGGCACACAGGCATTAGACAGAAAGCTGGAAGTTGAAATGGTGGAGTCCAACTTGCCTG<br />
GACCAGCTTAATGGTTCTGCTCCTGGTAACGTTTTTATCCATGGATGACTTGCTTGGGTAAGGACATGAA<br />
GACAGTTCCTGTCATACCTTTTAAAGGTATGGAGAGTCGGCTTGACTACACTGTGTGGAGCAAGTTTTAA<br />
AGAAGCAAAGGACTCAGAATTCATGATTGAAGAAATGCAGGCAGACCTGTTATCCTAAACTAGGGTTTTT<br />
AATGACCACAACAAGCAAGCATGCAGCTTACTGCTTGAAAGGGTCTTGCCTCACCCAAGCTAGAGTGCAG<br />
TGGCCTTTGAAGCTTACTACAGCCTCAAACTTCTGGGCTCAAGTGATCCTCAGCCTCCCAGTGGTCTTTG<br />
TAGACTGCCTGATGGAGTCTCATGGCACAAGAAGATTAAAACAGTGTCTCCAATTTTAATAAATTTTTGC<br />
AATCCATCAAAAAAAAAAAAAAAAAA</dnaseq><br />
==Labs working on this lncRNA==<br />
*European Molecular Biology Laboratory, Heidelberg, Germany<br />
*Institute for Science and Technology in Medicine and School of Life Sciences, Huxley Building, Keele University, Keele, United Kingdom<br />
*King's College London, Department of Haematological Medicine, The Rayne Institute, London, United Kingdom (F.F.)<br />
<br />
==References==<br />
<references><br />
<ref name="ref1"> Schneider C, King RM & Philipson L. Genes Specifically Expressed at Growth Arrest of Mammalian-Cells[J]. Cell. 1988, 54(6):787-793.<br />
</ref>(1)<br />
<ref name="ref2"> Coccia EM, Cicala C, Charlesworth A, Ciccarelli C, Rossi GB, Philipson L et al. Regulation and Expression of a Growth Arrest-Specific Gene (Gas5) during Growth, Differentiation, and Development[J]. Mol Cell Biol. 1992, 12(8):3514-3521.<br />
</ref>(2)<br />
<ref name="ref3"> Mourtada-Maarabouni M, Hedge VL, Kirkham L, Farzaneh F & Williams GT. Growth arrest in human T-cells is controlled by the non-coding RNA growth-arrest-specific transcript 5 (GAS5)[J]. J Cell Sci. 2008, 121(7):939-946<br />
</ref>(3)<br />
<ref name="ref4"> Smith CM & Steitz JA. Classification of gas5 as a multi-small-nucleolar-RNA (snoRNA) host gene and a member of the 5 '-terminal oligopyrimidine gene family reveals common features of snoRNA host genes[J]. Mol Cell Biol. 1998, 18(12):6897-6909<br />
</ref>(4)<br />
<ref name="ref5"> Mourtada-Maarabouni M, Pickard MR, Hedge VL, Farzaneh F & Williams GT. GAS5, a non-protein-coding RNA, controls apoptosis and is downregulated in breast cancer[J]. Oncogene. 2009, 28(2):195-208.<br />
</ref>(5)<br />
<ref name="ref6"> Mourtada-Maarabouni M, Hasan AM, Farzaneh F & Williams GT. Inhibition of Human T-Cell Proliferation by Mammalian Target of Rapamycin (mTOR) Antagonists Requires Noncoding RNA Growth-Arrest-Specific Transcript 5 (GAS5)[J]. Mol Pharmacol. 2010, 78(1):19-28.<br />
</ref>(6)<br />
<ref name= "ref7"> Kino T, Hurt DE, Ichijo T, Nader N & Chrousos GP. Noncoding RNA Gas5 Is a Growth Arrest- and Starvation-Associated Repressor of the Glucocorticoid Receptor[J]. Sci Signal. 2010, 3(107).<br />
</ref>(7)<br />
<ref name= "ref8"> Tani H, Mizutani R, Salam KA, Tano K, Ijiri K, Wakamatsu A et al. Genome-wide determination of RNA stability reveals hundreds of short-lived noncoding transcripts in mammals[J]. Genome Res. 2012, 22(5):947-956<br />
</ref>(8)<br />
<ref name="ref9"> Zhang X Q , Sun S , Lam K F , et al. A long non-coding RNA signature in glioblastoma multiforme predicts survival[J]. Neurobiology of Disease, 2013, 58:123-131.<br />
</ref>(9)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=Lnc-EPCAM-1:2&diff=1276473Lnc-EPCAM-1:22019-08-13T01:54:13Z<p>Qianpeng Li: </p>
<hr />
<div>''BCYRN1''-The shortest, long, non-coding RNA associated with cancer<br />
<br />
==Annotated Information==<br />
Approved symbol: ''BCYRN1''<br />
<br />
Approved name: ''BCYRN1'' : brain cytoplasmic RNA 1<br />
<br />
Alias symbols: BC200, BC200a, NCRNA00004, LINC00004<br />
<br />
HGNC ID : HGNC:1022<br />
<br />
RefSeq ID: NR_001568<br />
<br />
LncBook ID: HSALNT0289486<br />
<br />
===Characteristics===<br />
''BCYRN1'' is a shortest known long noncoding RNA with a length of 200bps<ref name="ref3" />.<br />
''BCYRN1'' is sense-transcribed from its gene locus situated on human chromosome 2 between the protein-coding genes for calmodulin 2 (CALM2) and epithelial cellular adhesion molecule (EPCAM)<ref name="ref1" /><ref name="ref2" />.<br />
''BCYRN1'' is relatively recent, no orthologs of ''BCYRN1'' have been identified outside of the primate order <ref name="ref8" />.<br />
''BCYRN1'' is found in the primate brain, Among neural cells, ''BCYRN1'' is highly expressed in dendrites, where is it thought to play a role in local translational control <ref name="ref3" />.<br />
''BCYRN1'' is a tissue-specific Pol III transcript, altering the view that Pol III was only responsible for the synthesis of transfer RNA (tRNA) and 5 S ribosomal RNA <ref name="ref4" /><ref name="ref5" /><ref name="ref6" />.<br />
''BCYRN1'' RNA sequence revealed three distinct sequence domains: a 5′ Alu element, a central adenosine-rich region and a 3′, 43-nucleotide, unique region containing a cytosine-rich stretch <ref name="ref7" />.<br />
''BCYRN1'' has a 5′ Alu element that has very high sequence homology to the Alu-J repetitive element found in the human genome and the Alu domain of 7SL RNA <ref name="ref7" />.<br />
<br />
===Function===<br />
''BCYRN1'' is important in several key features of cancer – like cell proliferation, survival and migration <ref name="ref3" />.<br />
''BCYRN1'' may act as a linker between certain proteins and mRNAs, allowing transient regulation and/or modification <ref name="ref3" />.<br />
''BCYRN1'' exerts its translational inhibitory effects by acting as a competitor for PABP <ref name="ref9" />.<br />
''BCYRN1''and BC1 interfere with eIF4A's catalytic mechanism by blocking the factor's helicase activity, while enhancing its ATPase activity <ref name="ref10" />.<br />
''BCYRN1'' is linked wit necrosis <ref name="ref3" />.<br />
<br />
===Regulation===<br />
TATA box and internal promoter elements play a critical role in transcription of ''BCYRN1'' <ref name="ref3" />.<br />
<br />
===Expression===<br />
long noncoding RNA ''BCYRN1'' is expressed predominantly in different regions of the brain. It also shows low level expression in testis but not in other normal tissues examined <ref name="ref3" /> <ref name="ref7" />. <br />
''BCYRN1'' is disregulated in cancer and is expressed in a number of human tumours but not in corresponding normal <ref name="ref3" />.<br />
''BCYRN1'' expression decreases with aging but is upregulated in Alzheimer's disease (AD). In AD affected brain regions, expression increased with disease severity <ref name="ref3" />.<br />
''BCYRN1'' also suggested to localise to dendrites <ref name="ref3" />.<br />
===Evolution===<br />
''BCYRN1'' arose after ''Anthropoidea'' diverged from prosimians and is conserved in ''Anthropoidea''<ref name="ref11" />.<br />
<br />
===Disease===<br />
*Alzheimer's disease <ref name="ref3" /><br />
*Breast cancer <ref name="ref3" /><br />
*Cervix cancer <ref name="ref3" /><br />
*Colon cancer <ref name="ref3" /><br />
*Lung cancer <ref name="ref3" /><br />
*Oesophagus cancer <ref name="ref3" /><br />
*Ovary cancer <ref name="ref3" /><br />
*Parotid cancer <ref name="ref3" /><br />
*Stomach cancer <ref name="ref3" /><br />
*Tongue cancer <ref name="ref3" /><br />
===Sequence===<br />
>gi|618|ref|NR_001568.1|Homo sapiens brain cytoplasmic RNA 1 (BCYRN1), long non-coding RNA<br />
<dnaseq>GGCCGGGCGCGGTGGCTCACGCCTGTAATCCCAGCTCTCAGGGAGGCTAAGAGGCGGGAGGATAGCTTGA<br />
GCCCAGGAGTTCGAGACCTGCCTGGGCAATATAGCGAGACCCCGTTCTCCAGAAAAAGGAAAAAAAAAAA<br />
CAAAAGACAAAAAAAAAATAAGCGTAACTTCCCTCAAAGCAACAACCCCCCCCCCCCTTT</dnaseq><br />
==Labs working on this lncRNA==<br />
*School of Biochemistry and Cell Biology, Western Gateway Building, University College Cork, Cork, Ireland<br />
*Department of Clinical Laboratory, Qilu Hospital, Shandong University, Jinan, Shandong Province, China<br />
*Department of Laboratory, Yuhuangding Hospital, Qingdao University Medical College, Yantai, Shandong Province, China<br />
*Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China<br />
*Clinical Medicine of Undergraduate, Taishan Medical University, Taian, Shandong Province, China<br />
*Wakayama Medical University, Wakayama, Wakayama, Japan<br />
<br />
==References==<br />
<references><br />
<ref name="ref1"> Basile V., Vicente A., Martignetti J.A., Skryabin B.V., Brosius J., Kennedy J.L. Assignment of the human BC200 RNA gene (BCYRN1) to chromosome 2p16 by radiation hybrid mapping. Cytogenet. Cell Genet. 1998;82:271–272. <br />
</ref>(1)<br />
<ref name="ref2"> Ludwig A., Rozhdestvensky T.S., Kuryshev V.Y., Schmitz J., Brosius J. An unusual primate locus that attracted two independent Alu insertions and facilitates their transcription. J. Mol. Biol. 2005;350:200–210.<br />
</ref>(2)<br />
<ref name="ref3"> Samson J, Cronin S & Dean K. BC200 (BCYRN1)–The shortest, long, non-coding RNA associated with cancer[J]. Non-coding RNA research. 2018.<br />
</ref>(3)<br />
<ref name="ref4"> Martignetti J.A., Brosius J. BC200 RNA : a neural RNA polymerase III product encoded by a monomeric Alu element. Proc. Natl. Acad. Sci. Unit. States Am. 1993;90:11563–11567.<br />
</ref>(4)<br />
<ref name="ref5"> Dieci G., Fiorino G., Castelnuovo M., Teichmann M., Pagano A. The expanding RNA polymerase III transcriptome. Trends Genet. 2007;23:614–622.<br />
</ref>(5)<br />
<ref name="ref6"> White R.J. Transcription by RNA polymerase III: more complex than we thought. Nat. Rev. Genet. 2011;12:459–463.<br />
</ref>(6)<br />
<ref name="ref7"> Tiedge H., Chen W., Brosius J. Primary structure, neural-specific expression, and dendritic location of human BC200 RNA. J. Neurosci. 1993;13 2382 LP-2390.<br />
</ref>(7)<br />
<ref name="ref8"> Martignetti J.A., Brosius J. BC200 RNA : a neural RNA polymerase III product encoded by a monomeric Alu element. Proc. Natl. Acad. Sci. Unit. States Am. 1993;90:11563–11567.<br />
</ref>(8)<br />
<ref name="ref9"> Khanam T., Rozhdestvensky T.S., Bundman M., Galiveti C.R., Handel S., Sukonina V. Two primate-specific small non-protein-coding RNAs in transgenic mice: neuronal expression, subcellular localization and binding partners. Nucleic Acids Res. 2007;35:529–539.<br />
</ref>(9)<br />
<ref name="ref10"> Lin D., Pestova T.V., Hellen C.U.T., Tiedge H. Translational control by a small RNA: dendritic BC1 RNA targets the eukaryotic initiation factor 4A helicase mechanism. Mol. Cell Biol. 2008;28:3008–3019.<br />
</ref>(10)<br />
<ref name="ref11"> Kuryshev V Y , Skryabin B V , Kremerskothen J , et al. Birth of a gene: locus of neuronal BC200 snmRNA in three prosimians and human BC200 pseudogenes as archives of change in the Anthropoidea lineage[J]. Journal of Molecular Biology, 2001, 309(5):0-1066.<br />
</ref>(11)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=LINC00574&diff=1276472LINC005742019-08-13T01:52:06Z<p>Qianpeng Li: </p>
<hr />
<div>''LINC00574'' is a lincRNA that is associated with chemoresistance in primary breast cancer.<br />
==Annotated Information==<br />
===Name===<br />
Approved symbol: ''LINC00574''<br />
<br />
Approved name: long intergenic non-protein coding RNA 574.<br />
<br />
Previous symbols: C6orf208.<br />
<br />
Alias symbols: FLJ13162, dJ182D15.1, CRALA.<br />
<br />
HGNC ID: HGNC: HGNC:21598<br />
<br />
RefSeq ID: NR_026780<br />
===Characteristics===<br />
<br />
===Function===<br />
[[File:Linc00574.png|right|thumb|400px|''LINC00574'' silencing in chemoresistant breast cancer cells resensitizes cells to chemotherapy<ref name="ref1" />.]]<br />
* ''LINC00574'' might be a target to reverse chemoresistance in breast cancer patients.<ref name="ref1" />.<br />
<br />
===Regulation===<br />
<br />
===Diseases===<br />
Primary breast cancer<ref name="ref1" />. <br />
<br />
===Expression===<br />
<br />
Non-responding tumors (poor response to chemotherapy, 32 samples) had fourfold higher ''LINC00574'' expression than responding tumors (good response to chemotherapy, 47 samples). ''LINC00574'' is upregulated in chemoresistant breast cancer cell lines compared to their parental lines<ref name="ref1" />. <br />
<br />
{| class='wikitable' style="text-align:center"<br />
|-<br />
! | Experiment<br />
! | Forward primer<br />
! | Reverse primer<br />
|-<br />
| rowspan="1"|Quantitative PCR<br />
| | 5'-CTCACTCCTCTGCCGATGCT- 3'<br />
| | 5'-CCACACCAGGACCATTCTCTTG 3'<ref name="ref1" /><br />
|-<br />
|}<br />
<br />
===Evolution===<br />
<br />
===Sequence===<br />
>NR_026780.1 Homo sapiens long intergenic non-protein coding RNA 574 (LINC00574), long non-coding RNA<dnaseq>GTGCTTGACTGGAGGAGGGCTGGCAGCAGAAGTGCAGCTGACCGGGTTGCGTTTTCGTACGGCTGACTAAAGCGGATACCGGTGGCGACTCATTTCTCGTTTTATTTTTCAACGATTTGGCGGAGAAGCTCCTCTTGTGA<br />
ATGGACTTTGGATTTCTTGGAGCTGCGCTGCGGGTCCCACAGTGTGGCTTTCGGCCCGTGCTGTGCTGGC<br />
GCCTGCACTTCCTCTGGCGGGGCACGGGGTGGCGCTCCCTGGTAAAGCAGCGGCCAGGGGGAGCCGTGAG<br />
TGAGGCGCTGCCTCTCCCGCTGAAGCGGGTTCCAAGGCCACCGTGAGGGGGACCATCCATCCAGGAGAGT<br />
ACTGGGCAGGCTGCAAATGTCTGTGTTAAAACAGCTCTGCTGGGCTAAGACAGGACAGAAGCAGACAGCA<br />
GGTGGATGAGACACAATTTCCTATCCAGCAGAACCTGCAGCAAGCTCCACAGCACCCTCCATGGGCTCAG<br />
TCTTGCTCCCGGGAAGATGGTTAATTCCATCAGCTCCTTCTGGCCGGCAGCAGGAAGAGTGGCCCTGTGT<br />
GTGCCAGGCCCTGCAGTCTCTCCTCTCAGCTGGTGTCTCCAGTGAGGGACCTGAGTCATCGCACACATGA<br />
GCCTGTGCTCAGCCTGCACATCTCCCGCCTCCCACCAGCTGCTCCTCAACTGCCAGGGCCAGACTGTGGC<br />
AAAATCTCACTCCTCTGCCGATGCTGGGGTTTCCCTCGTGTCTGGGAGGTGGTGTGCTTGGTGGCCTGAG<br />
CACTGCAGTGAATCCATGTTTCCCTCCCAGCACCCTGTTCTGTCCTCCAACTTGGCCGACAGCTCTGGCC<br />
AGGGACGCAGCCCAGCTGGTGCCCACCCCGCACTCTGTCCATTTCATAAGAGCCCTTGGTTTCCTCACTT<br />
CCCTCAGATTTTGCCAAGAGAATGGTCCTGGTGTGGCCCAGAAAGGCCAGCGGGGTGCAGCCTGGGACTG<br />
AAAGCAGAGGCGGCTCTGGTGGGGAAAAAGTAGCTCTCCCAGCCTAGCCCTACTGGTGGGCGGCACCTCC<br />
TGGCTCCAGGCCATCTTTTGTCCCAGTCCTAGGTAAGAAAAACACAAACAAAAGCCAGTCCCATGGCACT<br />
CGAGAAGCAGGAGGCCGTTCCCTGACAGCAACATGCTGTGTGCACAGACACACGGGTGGACAGGAGGCAG<br />
AGCTCGGGGTTGCTGCGGAGCGGGCAGGACACTGGAGCGGCAGGCAGTGCGGACCCGCCGGGCAGCCGTG<br />
CACGGTTGTCGTCCTCAGCGGCAGGAGCCAGTTTGTTGCTCAGGGCCTTGTCTTTTTACAAAGAGCCCCA<br />
GGCCCCGGGGGCTTCTCTGGGTGCCTCTTTGCTGCCATGTCTGCACGCGGGCGGAGAGCAGACCAGGCTA<br />
CCGACCCTCTCGCTTTGCTGTCTTCACGTGGAAAAGCCAGTGTCGTAGCCCCAAAGGAGGGGAAACTGTA<br />
TTGATTTGGGGAGCCTCTATGTTGATTTCAAAACAGATTGTCTCCTGTGTTCTCAAAGACTGGAAGCGAA<br />
CCCCACAACCGCCTTAGGCCACAAAAGCTTTATCCTTTCTAATTAGCATCCCTGTGACCTGCTCTGCGCC<br />
CTGCAGATATTTTGCTCAGCCAGCCAGAAGGAGGGAGGCCAGACACCAGCCCCCACAGACCTGCGGCTGC<br />
GACCCCCTGCCTGGGGACGATGGGGTCGGGGTCCAGTAGCTGCCCCAGAAACAAGTGGGGCTGCAGGAGG<br />
CTGATGGTGAGCTTGGAGGTTGGCAGAATTCTAAATCTGGGCACTGCAGGGTCCCCACAGGTCACGACCC<br />
TACTCTGCTCCACCCAGGCTCCGGAGGACCTGAGCAGGAACCTCTGCAGGGGGGGCCCGGGGCTCCCTGT<br />
CCTCTCAGCAGCCGGCAGTGCTCCCTGACAGCCCGGGCCTCTCCCTCCAGTAGTTCGGTAGTTTGCTGTC<br />
ACCAACATGGCTGGGCCTGGGACAGGCTCCTCCTCTCCCTCCAGAAGCCAGGCAGTCCCTCCTGCCTCAG<br />
TTTCTCAGACTAGGCCGCCTCTCCCATCGCGAGACACTGAAGACCCTCAGCTGTTTCCATCTGCCCAGTC<br />
TGACTGCTGGATCGCCCTCTGTGTGCGTTGGTTTGCTGTGTTCTTGCTACTCGCCCTTGGATAAGATTTC<br />
TTCTCTACTCATGAAGCTGCGTGTCCTGGAGGGCAGGGCCGCACCTCACATGCATGTTGCCCACATAGCT<br />
CAGCAACAGATGCTCTCACGCTTGTTAAAAGTAAAACCGGGCCAGGCGCAGTGGCTCACGCCTGTAATCC<br />
CAGCACTTTGGGAGGCCGAGGTGGGTGGATCACCTGAAGTCAGGAGTTTGAGACTAGCCTGACCAACATG<br />
GAGAAATCCCGTCTCTACTAAAAATACAAAAAATTAGCTGGGCGTGGTGGCACATGCCTGTAATCCCAGC<br />
TACTCGGAGGCAGGAGAATTGCTTGAACCCAGGAGGCGGAGGTTGCGGTGAGCCAAGATCACGCCATAGC<br />
AATTGCACTCCGGCCTGGGCAACAAGAGCAAAACTCTGTCAAAAAG</dnaseq><br />
<br />
==Labs working on this lncRNA==<br />
* Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.<br />
* Breast Tumor Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Li Y , Wang B , Lai H , et al. Long non-coding RNA CRALA is associated with poor response to chemotherapy in primary breast cancer[J]. Thoracic Cancer, 2017.<br />
</ref>(1)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=ILF3-AS1&diff=1276471ILF3-AS12019-08-13T01:51:04Z<p>Qianpeng Li: </p>
<hr />
<div>''ILF3-AS1'', a lncRNA that is associated with melanoma.<br />
==Annotated Information==<br />
===Name===<br />
Approved symbol: ''ILF3-DT''<br />
<br />
Previous symbols: ''ILF3-AS1''<br />
<br />
Approved name: ''ILF3-DT'': ILF3 divergent transcript<br />
<br />
HGNC ID: HGNC: 27115<br />
<br />
Chromosome: 19p13.2<br />
<br />
RefSeq ID: NR_024333<br />
<br />
Ensembl ID: ENSG00000267100<br />
<br />
===Characteristics===<br />
<br />
===Function===<br />
<br />
* ''ILF3-DT'' promotes cell proliferation, migration, and invasion via negatively regulating miR-200b/a/429 in melanoma<ref name="ref1" />.<br />
<br />
===Regulation===<br />
<br />
===Diseases===<br />
Melanoma<ref name="ref1" />. <br />
<br />
===Expression===<br />
''ILF3-DT'' is up-regulated in melanoma tissues and cell lines<ref name="ref1" />.<br />
<br />
===Evolution===<br />
===Sequence===<br />
>gi|210147556|ref|NR_024333.1| Homo sapiens ILF3 antisense RNA 1 (head to head) (ILF3-AS1), long non-coding RNA<br />
<dnaseq>ATCTTACGCCCGTCGCCCTGAGTACGTTAGCGGAAATGGCTCCGAGAGGCTTTGACGCATGTGTACCTTTTTAGTGGCGGTATCTCGGCCGGGGATTTTCGGGCTCCAGTGGAGGTGGCTATGCTCACCCCATCTCCCTTGAGAGGCACAGAAGGTTAGAGATGTGTGCGAGGAACGGCCAGGTCCAGCGTCTCCTCGTTGCTGCCCCTTGAGCCCGGGACCGGCGCCAATGCGCGCCCGGGTTCTTGGGTTCTTTCGTCCCGCAGACCTGCCTTGGTGTGGCGTCCCTGGGCCGTAGCTTCCGAAGGCTGCAGCCGACCTGGTCGGGGTCCTCTAGCCCGCCTTCCCCTTCCCCCATTGACAGATGGAGAAACTGAGGCCCAGGCCAAAAAATATCTCACTAGAGGGCTCACCGCCATTTCCTGGAAAAATTGGGGCTGGGACTCAACGGACGCTCGTCCAGCAGCAGCGCGGAGCTCCGAAGTAAAGGCGCCCGTGACCGAGTGCTTTGTCCTTACAAGCGTGGTGTTCTTGAATGCTTCCAGGCGCCTTATGAGGCCCCCGATGTACAATCTGTGCTTAACTAAACCCCACTGTCTTCCAGGGTCAGGTTGGCCATCCGCAGGCGTAGTTGCTAGGAAGGTTTGACAGATGTCCGCCTGTTGATTCAGACGTTCCCAGGATTTGGAGCAAGAAGAGCAAGGAAGGCCAGGCGCGGTGGCTCACGTTTGTAATCCCAGCACTTTGGGAGGCCGAGGCGGGCGGATCACGAGGTCAGGAGTTCGAGACCAGCCTGGCCAGCATGGTGAAACCCCGTCTCTACTAAAAATACAAAAGAAAATTAGCCGGGTGTGGTGGCACATGCCTGTAGTCCCACCTACTTGGGAGGCTGAGGCAGGAGAATTGTTTGACCTGGCAGGCGGAGGTTGCAGTGAGCCGAGATTGCGCCACTGCACTCCAGTCTGGGCGACAGAGCGAGACTCTGTCTCAGAAAAAAAAAAGAGCAAGGAGGTGTTGAAAATGGGTTTCCTGGCTGGGCGTGGTGGCTCACGCTTGTAATCCCAGCACTTTGGGAAGCTGAGGTGGGCGGATCACTTGAGGTCAGGAGTTTGAGACCAGCCTGGCCAACATGGTGAAACACCGTCTCCACTAAAAATAGAAAAATTAACTGGGTGTGGTGGAGGGCGCCTGTAATCCCAGCTAATCAGGAAGCTGAGACAGGAGGATCGCTTGAACCCAGGAGGCGGAGGTTGCAGTGAGCCGAGATTGCTCCATTGCACTCCAGCCTGGGCGATAGAGTGAGACTCAGCCTCAAAAAAAAAAAAAAAAAAAAATTCGCCAGGTGTGGTGGTGTGCGCCTATAATCCCAGCTACTCAGGAGGCAGAGGCACAAGAATGGCTTGAATCACTTGAACCTGGGAGGCAGAGGTTACAATGAGCCGAGATGGCACCACTGCACTCCAGCCTGGGCGACAGAGCGAGACTCCGACTTCCCATCTTAAAAAAAAAAAAAAAAAAAAAAAAGAAGTGTAAAGATGTGATTATGTGGCAGGGGGTAAGGGTTAAAAAGAAAACAAGAACAAGTTTTCCTCTGCTTAGCCAGCTTACTTCAAGGACAGTTATAACACTGAAAAGTCGAGGCCAAAGGAATGGGCTCCAGACAGCCTCCTCCGGAGCAAAGTTGAAAAGAAAAATTCCTTTACTGTCTCTCCTTTTCTGAACCATTAAATATGACTGTTTGCCAATGGTTGTATTTAGTAAGATTTGTAGACTCTGTTTTTCTTTTGACACAGCTGCAAGGCCAACAGCTGTGCAAAGCCACAAGTTATGCTAAGTCAGCAGTTATGCTATAGATTACATGACCTGTGACTGTATCATTAACTGCTTTTGTTTTGCTTCTGTAAGTTTGCCTATAAAAACCACACTCAGTCTTTGTTCAATGGTCAGCTTTTCAGATACAAATCCACTGAGCCGGTGTACATCTAAATAAATCCTCCTGTTTCCCGTGTCAAAAAAAAAAAAAAAAAAAAAA</dnaseq><br />
<br />
<br />
==Labs working on this lncRNA==<br />
* Department of Burn and Plastic Surgery, The 253rd Hospital of PLA, Hohhot, Inner Mongolia 010051, China<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Chen X , Liu S , Gao G , et al. Long noncoding RNA ILF3-AS1 promotes cell proliferation, migration and invasion via negatively regulating miR-200b/a/429 in melanoma[J]. Bioscience Reports, 2017:BSR20171031.<br />
</ref>(1)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=NONHSAT084827&diff=1276470NONHSAT0848272019-08-13T01:50:18Z<p>Qianpeng Li: </p>
<hr />
<div>''TUG1'' is a promising biomarker and/or a therapeutic target for bladder urothelial carcinoma.<br />
<br />
==Annotated Information==<br />
===Name===<br />
''TUG1'': Taurine up-regulated 1 (HGNC nomenclature), also known as TI-227H; Linc00080; ncRNA00080 <ref name="ref1" /><ref name="ref9" />.<br />
<br />
LncBook ID: HSALNG0134930<br />
<br />
===Characteristics===<br />
''TUG1'' is three exon transcript of 7542 bp (GenBank) long non-coding RNA that is found on human chromosome 22q12.2 (HGNC) <ref name="ref1" />.<br />
<br />
===Function===<br />
[[File: TUG1.jpg|right|thumb|400px|'''''TUG1''-based signaling circuit in osteosar''' <ref name="ref10" />.]]<br />
<br />
* Required for the proper formation of photoreceptors in the developing rodent retina <ref name="ref1" />. Downregulation in developing retina leads to decreased retinal transcription factor expression and increased apoptosis <ref name="ref1" />. ''TUG1'' associates with PRC2 (polycomb repressive complex 2) and represses a number of cell cycle genes <ref name="ref3" />. Depletion of ''TUG1'' led to significant up-regulation of 120 genes, which were strongly enriched for those involved in cell-cycle regulation (regulation of mitosis, spindle formation, and cell-cycle phasing) <ref name="ref3" />.<br />
<br />
* ''TUG1'' promotes cells proliferation and inhibits cells apoptosis through regulating AURKA in Epithelial ovarian cancer (EOC) cells <ref name="ref8" />.<br />
<br />
* ''TUG1'' functions as a sponge for miR‐219a‐5p to upregulate PIK3CA levels in osteosarcoma cells. In addition, the activation of the AKT pathway promoted TUG1 expression by up‐regulating the expression of Forkhead Box M1 (FOXM1), forming a positive feedback loop in osteosarcoma <ref name="ref10" />.<br />
<br />
* ''TUG1'' regulate CELF1 by binding to PRC2 <ref name="ref11" />.<br />
<br />
* ''TUG1'' promotes migration and invasion by acting as a ceRNA of miR-335-5p(competing for miR-335-5P with ROCK1) in osteosarcoma cells<ref name="ref12" />.<br />
<br />
===Expression===<br />
Expressed in the developing retina and brain <ref name="ref1" />. Expressed in adult tissues with highest expression in cortex <ref name="ref1" />. Expression levels are elevated in the caudate nucleus of patients suffering from the trinucleotide repeat neurodegenerative condition, Huntington's disease <ref name="ref4" />. Localises to both the nucleus and cytoplasm <ref name="ref3" />. Transcript was classified as unstable with a half-life >4 hr in human Hela cells <ref name="ref5" />. Similar results were found in human B cells and mouse 3T3 cells <ref name="ref6" /><ref name="ref7" />.<br />
<br />
''TUG1'' is overexpressed in bladder urothelial carcinoma compared to paired histologically normal urothelium <ref name="ref9" />.<br />
<br />
''TUG1'' is downregulated in non-small cell lung cancer (NSCLC) <ref name="ref11" />.<br />
<br />
''TUG1'' is upregulated in gastric cancer. <ref name="ref13" />.<br />
<br />
{| class='wikitable' style="text-align:center"<br />
|-<br />
! | Experiment<br />
! | Forward primer<br />
! | Reverse primer<br />
|-<br />
| rowspan="1"|Real Time Quantitative PCR<br />
| | 5'-TAGCAGTTCCCCAATCCTTG-3'<br />
| | 5'-CACAAATTCCCATCATTCCC-3'<ref name="ref9" /><br />
|}<br />
<br />
===Conservation===<br />
Single highly conserved homolog of ''TUG1'' is present in human, mouse, cow, and dog genomes. <ref name="ref1" />. Present in two locations in rat, with one an apparent processed pseudogene.<br />
<br />
===Regulation===<br />
''TUG1'' is transcriptionally regulated by p53 in response to DNA damage <ref name="ref3" />.<br />
<br />
===Disease===<br />
* B-cell neoplasms <ref name="ref2" /><br />
* Bladder urothelial cancer <ref name="ref9" /><br />
* Epithelial ovarian cancer <ref name="ref8" /><br />
* Huntington's disease <ref name="ref4" /><br />
* Non-small cell lung cancer (NSCLC) <ref name="ref11" /><br />
* Osteosarcoma <ref name="ref10" /><ref name="ref12" /><br />
===Sequence===<br />
>gi|55000|ref|NR_002323.2| Homo sapiens taurine up-regulated 1 (TUG1), transcript variant 3, long non-coding RNA<br />
<dnaseq>TCCTGCTTTCCTGACCCTCTCCGCCATTTAAAGAAACAGTACCGGGGGCGGGCCGAGCGACGCAGCCGGG<br />
ACGGTAGCTGCGGTGCGGACCGGAGGAGCCATCTTGTCTCGTCGCCGGGGAGTCAGGCCCCTAAATCGAA<br />
GAAGCCCTGGCGCGCCCTCCCCCCCTCCCGGGTCTGGTAGGGCGAAGGAACGGGCGTGCGGTCGATCGAG<br />
CGATCGGTTGGCGGCTCTTTCTCCTGCTCTGGCATCCAGCTCTTGGGGCGCAGGCCCGGCCGCCGCGGCG<br />
CGCGCCCGGTGGCCGTTGGCGCTCGCGCCGCGTCTTTCTTCTCGTACGCAGAACTCGGGCGGCGGCCTAT<br />
GCGTTTGCGATTCGACGAGGAGTCGTCCGGGTGGTCGGCGGCGGCGGGCAGCTGCTCCGCCCCGCTCCGG<br />
GGGAGGCGGCGGCGGCAGCGGCCGCGGGATTTGGAGCGGCCGGGGAGGCGGGGGTGGCCGGGGCCGGCTT<br />
GGAGGCCTGGCGCCACCCTTCGGGGCCTGCAAGGACCCAGTTGGGGGGGCAGGAGGGGGCCGGAGGATGG<br />
TTGGTTGTGGGATTTCTACTTTGCCTTTTCCTCCTTATGCCGCCTTAGTGAGGGGCGGGAGCTCTGGCGG<br />
CAGCCCCGGGGTGGGGAGACGAGCTCCGGAGTCGGAAGAGCTGGGTTTTCTTCCGGGCCTAGCCACCAGT<br />
TGGCGGAGTGACCTTAGGCGAGTCACTCTGTAATTTGTCTGCGCCTCAGTTTCCTCCTCTGCCTATCAAT<br />
GTGTGTGGGGTTGAAATCGCTTTGTAAACTATAAAGCGTGGGTGTACGTAAAGGATGGTTATTGTTTATA<br />
ATTTTTTTTGAGTTGTAAGAAAACTTAGCAGTTCCCCAATCCTTGGGTTTTGAACCTGGGAACCTTGGAT<br />
TGGAGTTGGGGATCCCCAAACTTCCTGAAATTGTGGGAATGTGCGGTTTGGGGGAATGATGGGAATTTGT<br />
GGGAATGTGCGTTTTAGGGGAATGATGATCCATCGCTAGCAAGTTTTCCAAGGGGGCTGTGACCCAGAAG<br />
AGTTAAGAATCACAATTTCTTCATGCTACAGAGAGGAAACTGAGGCCTAGATGTCATTTGGGACCCTTCA<br />
CAACCATTTTGAAGCCCTGTTTGAGTCCCTGGGATATGTGAGCTGTTTCTATGCATAATGGATATTCGGG<br />
GTTAACAACAGTCCCCTGCTTGGCTTCTATTCTGAATCCTTTTCTTTCACCATGGGGTGCCTGAAGGGTG<br />
GCTGATGCATATGGTACAATGGCACCCAGTGTAAAGCAGCTACAATTAGGAGTGGATGTGTTCTGTAGCA<br />
TCCTATTTAAATAAGCCTATTTTATCCTTTGGCCCGTCAACTCTGTTATCTGCTGCTTGTACTGGTGCCT<br />
GTACTTTTCTGACTCTCATTGACCATATTCCACGACCATGGTTGTCATCCATTACTTGATCCTACTTTAC<br />
ATGTCTAGGCTGTGTGGTTGGTGGTGAATAGGCTTCTTTTTACATGGTGCTGCCAGCCCAGCTAATTAAT<br />
GGTGCACGTGGACTTTTAGCAAGCGGGCTCACTGGAAGAGACTGAACCTGGCATGGAATTCCTGAAGATG<br />
TTTGGGGTTTTTTTCTTTCTTAATCGAAAGTTAACATTGTCTGAAAAGTTTTGTTAGAACTACTGCGGAA<br />
CCTCAAAATCAGTAGATTTGGAAGTGATTCAAAGCTAAACTTTTTCCTTGGCCCTCCTTGTGTTCTAATT<br />
GCTTGCAAGTGTAATACTAGGATGTCCAAGATGCCAGTTTTTGCTTCTTTGTTAGTTGTCAGCTGCTTTT<br />
ATCAAATTTCAGGCCATTATCCAACAAACACTATAAAAATGTTTGAACAATTGGATTTCAAACATTTTCG<br />
TTTTGTGGAGTGGTGCTCACCAAGTGGTACAGCCCTAAGCAAGTGAACACAAACACATTTAAGTGTATTT<br />
TGTCTGATTAGATGTTAGCCAGTTATGCTATTTCATTCAAATGTCTGAAAAAATCAATTGACTATTCCCT<br />
TTTCCTAAAGGGCAGAGACAGATAATCTCACTTCCAGAGAAATGACTTGGAGAAAAAAAAGTGTTGGTCT<br />
TTTTGCTCTTTTGTAATTAAATCCGGATGTACCTCAAAAGACTTAAGACTGTGGTGATAAGATGCTTTCC<br />
TCAGCAGAAAGGAGGGAAAAAAAACAACTGGAACTCAAAGCTTGAAATTCTGTGGCAAAACATGAGATGT<br />
CCAGGATTGGAGGTTGAAAAGATTTCACTACAGTGTTCTGCAATAGTTGGAGCAGATAACTTTCAGTGTA<br />
GCCACAGCCATGGACTCCAGATTTCCAGATTTTCAAGACCTGGACCTGGAACCCGAAAGAGCTTGTCACG<br />
ATGCGGCAGGAACACTGGAGGTAGATTTTTTTTTATTTTTGAATTTTGGGACTGTTGACCTTGCTGTGAG<br />
AAAAGAGACAACGACTGAGCAAGCACTACCACCAGCACTGTTACTGGGAATTAGAAGACCTGAGTTTCTG<br />
TCCAGACCCTCAGTGCAAACTGAGGATGCTCCATCCAAAGTGAATTATGTCCTGTGCCTCCTGATTGCTG<br />
AGTGTTCACCTGGACCTTCTGACTACCTTCCCTGTGCTATTCCATCAGCCTACAGACCTGGTACCTGGAT<br />
TTTTGCCCGAGATGATTCCTACCACCTTACTACTGACGAAGACACCCATTCCAGTGGACCACTGTGACCC<br />
AGGAGGCATTCAGCCATCATGATGTGGCCTTTACCTCCACTCCTGTCTTGTTCTACCCAGATTCAGCACA<br />
GCCCTTTATAGTGAAGTCAGAGTCCTCAAGCCAAATAGCTAAAGCTGTTTTATCACAACAAAGGCCTAGT<br />
TTGTTCCATGAGTGTGCATTTCATTTCTTCAGTTAAAGCCTTCAGAGACACACAATAAATTTGGACCAGG<br />
GGATTTTTTAGTTATTAATGCTCTCTGAAGAAAGGCAACATCTTTTTGAGAGCAGCATTGGACCACACCC<br />
CACAATCTCAAATGATTGAAATTCATGAACATCTAGGATCCCGTGAAGGTCACTGGACCCTGTTTTTTCT<br />
ACTTCAAATCCTGTAGTAGCCTACTGAATGAGAAAACATATTCTGACCCATTGGGATCAAATCAAAGGCA<br />
CAGTGAACTCCTCATAGCATCTTCTTTGGAATTACTCAGGAACCAGAACTTTTTACACAAATGTAAGAAA<br />
TTCTACCAAGGAGTCCCCTTACCTAACAGCATCTCACAAGGCTGCACCAGATTCCAGAAAAGGCTTCTCT<br />
TGATACATCAAGGTAGAACCTCTATGCATTTTGTGACCGACTTATTCTTAGATCATTGGTTTTCCAAAGG<br />
CTTTGTGGCCATGAAGCCCTTTGAGTGAAAACTGTGCAGAAGCCCAGAGTAAAAGTGAAGCTGCTCTGGA<br />
TGAAGTAGTGAAGCAAGAGTAGGGGCCTGAATCCTGCTACAACTATCTTCCTTTACCACCGTGGTGACAC<br />
CTAAGGGGACTTCCTTACAACACCTTGAACTCTTCCGAACACAGTTTGAAAACCACTGCCCCAGACAGCA<br />
ATATGTTTGACCTGAATGGCATTCCAATCTTTTCTGTACCTCCACTCAGCACAGTTCATGTTCAGTAGAT<br />
GCTGAACATTCTTAGAAATACTGTGTGTGAACTTAGAAAAGTGCAAGAAGACAGGCATGTCTTTGACCCC<br />
AGGAATGATCATTTGCTGAAGATGGTGTCAAGTGAACCTAGATTAACAGCCCTCCACTCCAGATGGATAT<br />
CCAGTGATTCCTAGAATGGGATATAGCCAGAGAACAATTCTATGCACCCTACACTGACAGACTCCCTTAA<br />
GCAACACCAGATGCTCTACTGGTACTTGAAGTACATGACTTTGAAGTCTTGACCCTCCATGAATACCTGA<br />
ATTATCAGCAAGCGGGTTTTGAAGCTGGTGCCTCATTGAGGCCATATTAGAGCAACTTGTACATTTGACC<br />
TCTTGTTATCAGCCATGGTACTCTACTTCGTGTGCAAGAGATAACTATGAAAGCCAAATTCAAATACTGG<br />
CAACATTTCCTAAAGGGGCTCAATATCTATCATTCGTCTTCTTTTCCAAACTACACATCACTGTATGACT<br />
CAACCAGTAGCAGTTATATTGCCCCTTGGTTTTTATTCAGTTTAACTACTGTTTCCAAGATAAATGAGCT<br />
AATAAGCTTTAAAAAAAAAAAAAAAAAAGGCTGAATTCTTTTTTCTTCATCACTGGCATATCTGCCTATT<br />
CTCCAGAATTATTATGACTATTCAGCTCACTTTAACAGTTGAACTTCAAGCGACAATCTTTGAACACCCC<br />
TTCTCATGTGATTTAAAATGAAACCATTTGGAAAAGTTTCTTCTAGCCAGTAATAGATTTTTTTTTTAAT<br />
TGCTCTGCCTTGTGCCGAGAGATGTTCTTTTAAGATGAATCTTTTGATGTCTGATACCACCAAATATAGG<br />
TGGTAGGGAGAGTTGGAGGCTGGCCCTTTGAGCAGGCCATTAGCTTACTTGCTGGGCATTTCCGATAGCT<br />
TATTGCCTACCTTTTTGCTGGAAACAAACTGATTTGAAAAACAAAATCTATGAAGACTGCAGCTAAGGAT<br />
TTTATCGGTAGACTTAAGAGCTTTTGTCCTTGTGGATATTTTAGTGGAACCACATCAGTCTCAATACTGT<br />
CATTTTACACTGACTCAGAGCAGCTGACTTCATTCCTTGCCATGATATATATTTAAGGCAGGCATTGTAA<br />
CAGACATAAAGACAACTTATCTGTTTCAGCAGGAAGGATTCAGTTTATGAACTCTCAGACCAGATCATGT<br />
TGAACAAGGAGACTTTGATGTGTGTCATGAGAAAACTCATTCTTTACTTCCCAGTCAATTTAAAGGCCAG<br />
CTATCCTGAGCTACTCGAATGAATGCACTGGTTAAACATTGGAAATAGTTTGTTTATATCCTTGTCTCTC<br />
TCTAGGCCAATTGTGATTACATGACTCGACTCTACATCTCGTCAAACAAGGCCTAGGTCTGGTTGCTGTA<br />
GACTGCTCGCCCTCAACAAATAAAATCTGGTTGACTAGCCTCCTTGTATATACAACTATTATTTGTTAAG<br />
AAGAAATTATCGTCAATTTTCTACTACCTTCCAATTGTCAGCTCTTTTTTTCCTCTCTGGTTTTTCCTAT<br />
ACTTTACAGAAAAAGACATTGATCTATACTGCCATTCCCTCTAATCCTGCCATACTCAGTCAAAAGGAAT<br />
GACTTAAGATGAAGATGATCATCTGCTCGAGTCTAAAATATACATTGTATATAAGAATTGGTGATTAGAA<br />
AAGCAAAAAACCTAAAACTTAAATCTAGGAGTCTGTATACTGTCTCCATGTCTCCATGCCTCAGATCTCA<br />
TCTAAATCTTTGAACAGCACCATTCAACCAATCTGAGGCCTTGACTTGCTTGTAAGATGATTCTCAGAGA<br />
TCGGCTGAGTTAAAAAAGATGACGACTTGATTACCAAAGAAAGTAGGGCCAACTTTGACAAATCTGGCTC<br />
TGCTGACCCTGTCACTCCCAGATGTAGCATAGACTCCTAAACAGAACCTCAAGTCTGATTGAGGATAAGG<br />
CCTTCTCCTGAGCTGAAAGTTCTTTGGCAGATGAGCAAGAAACTGAAAGCTGATGTACCTGACTGGCTCT<br />
GTAAGATCAGAAAACTGTATCCAGAATAAGCCCTATGGATTAACCCCTGAGTACCCAGAGTAAAAACTAA<br />
TTTACAGAACTTCCTTATTGATCTGCTGGTTCTTCCAGATCATATTCTGGCTATTGGTATGGCTGGCCTT<br />
TCTGAAGGTACCCTGCTTGTCTATTTTCCTGACTCAGCTCTTGCCTGCCTTTTTCACATGTTGCTGCAAT<br />
TAGACTCACCGTGAGGACTACAGTCAATTTCAGTCTATCTTGTGCCCAATACAACAAGGATTTTTAATAG<br />
TAACAACCCACACCTCACCCACTAGGACTCAATGTTCACAACAGGAAGGACCATTGCTGCATACTCCTTG<br />
ACCAGCAACTTTTTTGAAGATATTTTTAAGTGCAGAGTAGGCCTCTATTCCTGTATGTAATTGTTCATTT<br />
TCAGCACCTGGAACCTCATCTATCGGGTCTGGAAGGAATACAGCAGTTCGAAAGCCGCGTCCATTTCTCT<br />
CCTTCAGTAGTGCAGAAATGAGTCCGATTCACCAGTACACACAGAACTGTACCAGTTCAACCTAGCAAAA<br />
GAAGAAAAGTTTCCACTGTACTTAAAATTTACAGCTGACTCAAATTGCCTCACAGAATTATTTGATGTAG<br />
AAGGCTAGTTGTCTTACTTCAGATCAGCAGGACAGTTGGGCTCTCAGACTCATGACCACTGAGTTTGCTT<br />
GTGTTGAAACTGTGGTTTCATCCAACATATGCTATTGGACATGATTATTATTCCATTCAAATGGATTACA<br />
GACTTCTTGAGGACAGGACAAACTTATCTCTCATGGTGTTTTTTTAGAATACTTTTATAACCAAGGAAGA<br />
AACCATGCCAGCTGTTACCATTCAACTTCTTAAGCAGAGATTAAGCTTTTTCATATCTGTTCTTATCCTG<br />
GACATCAGTAGTTTTTAATTGCCCAGCATCCGTTCCATCTTGTAACAACTCCCTGATGTTTCTTAAAACC<br />
ACCTCTTCCTATTTTCAGTCTGTGGTTTGGACAGTCTGACCCAACCTTGAGCTTTGTGGGTGAACATGTA<br />
ATTCAGACCTCATCAATCAGCAAATCCATCTGAACTGTGGAGGAGAAGCTCTCTTTACTGAGGGTGCTTT<br />
AGCTTTGTAGGATGAAAACCTCAAACTAACAGGGCCTACCATGTAGAGAATGAAGCCAGTGCAGGGGAAA<br />
GCAGAGCCAAAATATGGAGAGACTTGAATCCTGATGACAGCGTTTGTGCCCCTGGATCCAACCGTGCCTG<br />
AAGCTAGAATATCCCCTGGACTTTTCAGTTATGTGAACCAATAAATACCCTTTTTTGCTTAAGTTACTTT<br />
GAGTTGGGTTTCTGTTACTTGAAATTGAATCCACACTAATATATCTACCAACATTGAGACTTGACAGATC<br />
CAAGTATTTATTAAGCTAGAGGTCATGGTCACTGAAATTACTTTCCAAAGTGGAAGACAAAATGAAACAG<br />
GAACTGAGGGAATATTTAAGATCCCACAGAAGCGTAAAAATGACATGGTAGAAAGTAATAGAAAACCTAA<br />
ATGTCTGTCATTAAAGGATAGGTTAAGGTGTGGTTCAGCCATATAGGAATATCTCGTATCTGTTAAAATG<br />
AATAAAGTACATTCATTGTGTATGGAAAAATGGCCATGATACATTAGGTGAAACAAGTTATTAATAGAAA<br />
AGTGTACAGTGTGAACTCATTTTAAAATGTGTGTGCTTATGTTTATAAATGCATAGAAAGGTCTATTCAC<br />
AGCTTTCTTTGAACAGTGTAGATCACATGAAACTTTCAACTTTATACATTTCTGTATTAATATTTTACAC<br />
TACCCACATTATTTTTAAACTTTATTTTAAATAAAGAATTTTTAAAATTAAA</dnaseq><br />
==Labs working on this lncRNA==<br />
* Department of Imaging, People's Hospital of Lishui City, the Sixth Affiliated Hospital of Wenzhou Medical University, Lishui, China. <ref name="ref8" /><br />
* Department of Gynaecology and Obstetrics, People's Hospital of Lishui City, the Sixth Affiliated Hospital of Wenzhou Medical University, 15 Dazhong Street, Liandu District, Lishui 323000, China.<ref name="ref8" /><br />
* Guangdong Key Laboratory of Male Reproductive Medicine and Genetics, Peking University Shenzhen Hospital, Shenzhen, China.<ref name="ref9" /> <br />
* Institute of Urology, Shenzhen PKU-HKUST Medical Center, Shenzhen, China.<ref name="ref9" /><br />
* Central Laboratory, Shenzhen Second People’s Hospital, Shenzhen, China.<ref name="ref9" /><br />
* Department of Orthopedic Surgery, the First Affiliated Hospital of Harbin Medical University, Harbin, China.<ref name="ref10" /><br />
==References==<br />
<references><br />
<ref name="ref1"> Young TL, Matsuda T, Cepko CL. The noncoding RNA taurine upregulated gene 1 is required for differentiation of the murine retina[J]. Current biology, 2005, 15(6):501-512.<br />
</ref>(1)<br />
<ref name="ref2"> Isin M, Ozgur E, Cetin G, Erten N, Aktan M, Gezer U et al. Investigation of circulating lncRNAs in B-cell neoplasms[J]. Clinica chimica acta. 2014, 431:255-259.<br />
</ref>(2)<br />
<ref name="ref3"> Khalil AM, Guttman M, Huarte M, Garber M, Raj A, Morales DR et al. Many human large intergenic noncoding RNAs associate with chromatin-modifying complexes and affect gene expression[J]. Proceedings of the National Academy of Sciences. 2009, 106(28):11667-11672.<br />
</ref>(3)<br />
<ref name="ref4"> Johnson R. Long non-coding RNAs in Huntington's disease neurodegeneration[J]. Neurobiology of disease. 2012, 46(2): 245-254.<br />
</ref>(4)<br />
<ref name="ref5"> Tani H, Mizutani R, Salam KA, Tano K, Ijiri K, Wakamatsu A et al. Genome-wide determination of RNA stability reveals hundreds of short-lived non-coding transcripts in mammals[J]. Genome research. 2012:gr.130559.111.<br />
</ref>(5)<br />
<ref name="ref6"> Friedel CC, Dölken L, Ruzsics Z, Koszinowski UH, & Zimmer R. Conserved principles of mammalian transcriptional regulation revealed by RNA half-life[J]. Nucleic acids research. 2009, 37(17):e115-e115.<br />
</ref>(6)<br />
<ref name="ref7"> Clark MB, Johnston RL, Inostroza-Ponta M, Fox AH, Fortini E, Moscato P et al. Genome-wide analysis of long noncoding RNA stability[J]. Genome research. 2012.<br />
</ref>(7)<br />
<ref name="ref8"> Li T, Chen Y, Zhang J & Liu S. LncRNA TUG1 promotes cells proliferation and inhibits cells apoptosis through regulating AURKA in epithelial ovarian cancer cells[J]. Medicine. 2018, 97(36):e12131.<br />
</ref>(8)<br />
<ref name="ref9"> Han Y, Liu Y, Gui Y, Cai Z. Long intergenic non‐coding RNA TUG1 is overexpressed in urothelial carcinoma of the bladder[J]. Journal of surgical oncology. 2013, 107(5):555-559.<br />
</ref>(9)<br />
<ref name="ref10"> Li Y, Zhang T, Zhang Y, Zhao X, & Wang W. Targeting the FOXM1‐regulated long noncoding RNA TUG1 in osteosarcoma[J]. Cancer science. 2018, 109(10):3093.<br />
</ref>(10)<br />
<ref name="ref11"> Lin PC, Huang HD, Chang CC, Chang YS, Yen JC, Lee CC et al. Long noncoding RNA TUG1 is downregulated in non-small cell lung cancer and can regulate CELF1 on binding to PRC2[J]. BMC cancer. 2016, 16(1):583.<br />
</ref>(11)<br />
<ref name="ref12"> Wang Y , Yang T , Zhang Z , et al. Long non-coding RNA TUG1 promotes migration and invasion by acting as a ceRNA of miR-335-5p in osteosarcoma cells[J]. Cancer Science, 2017.<br />
</ref>(12)<br />
<ref name="ref13"> Cao W J . Analysis of long non-coding RNA expression profiles in gastric cancer[J]. World Journal of Gastroenterology, 2013, 19(23).<br />
</ref>(13)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=SNHG31&diff=1276469SNHG312019-08-13T01:48:13Z<p>Qianpeng Li: </p>
<hr />
<div> <br />
==Annotated Information==<br />
===Name===<br />
Approved symbol: ''SNHG31''<br />
<br />
Approved name: ''SNHG31'' : small nucleolar RNA host gene 31<br />
<br />
HGNC ID: HGNC: 54196<br />
<br />
Ensembl ID: ENSG00000229267<br />
<br />
RefSeq ID: NR_110292<br />
===Characteristics===<br />
<br />
===Function===<br />
<br />
<br />
===Diseases===<br />
<br />
<br />
===Expression===<br />
<br />
===Evolution===<br />
<br />
===Sequence===<br />
>NR_110292.1 Homo sapiens small nucleolar RNA host gene 31 (SNHG31), long non-coding RNA<br />
<dnaseq>AAGCCCCTCTGGGCTGCCTGGACGGATGAAGTCCAGGTGGAAAGCCAGTCGACGTTTCCCGGGAGCTACG<br />
ACTCCAGGGACCCTCATCCGAGCTTAACCGTTGGAACAATCACAAACCCAGAAACTTTTAGCTGAGTGTT<br />
ATTTATAAAAAGCGCTGTTTTGACTGCTGTTGGACTTGGAAAAGCTTTGCCCACGATACTGAAGCGTAAT<br />
TAGCTGCCTACTTTTCAAAATTATGTGATGACTTCATGGGAAAAGAGATTCACAAGAACCAGTAACAGGA<br />
AAGCTTAAATAAGCTTGGAAATCTTTAAACTTTCAATATCGATTGAACTTTTTGCTGCATTACCACAAGA<br />
TTCTCTAGTAAGGCTTAATAGAGCTGAAACAGAATTCACAAGACAGGATTCTCACTGACTGTTACCCCTG<br />
CGTCCTCTTTCTCCTTACTGAGGGGAAAATGCCAAAGCAATTGGGGAAAAAAATACTGTTTTCTCTGAAA<br />
TGAAGACTCCTCAAGATCCTGTTGCTGGAATGAGTATTGGACTCTTCGGTCTACTTCTACAGTCACCAGT<br />
ACATCTGGCATACACTATGATGCCCAACAGTAGGAAGATGAAAGAAATGTAGATGTTGGCATTTCTAAAA<br />
GAGATGTTGTATCTTTTTTCCTACTTAATAGACTATTAGGCTATAAATCTCAATCTTGGCCAGCAAATGT<br />
GTTTGCCAGCTTTTCTTTATTCTTTTTAATTTTTTTGAGGATCAGCATGGAAAAACAATTTGCGCAAGGC<br />
TCAAGAAGATGAGATGGTCTTATAAACAGTAATTGAAATATGTATATTTTTTAAAAGTCTGTTTCAAATT<br />
TCAAACCTTATTTTAAAAACTATGTGAAAGCCTCTTGTGAAACTCAACTGAAGTAGGCATGGCTGAGTCC<br />
AGAGGAGCAGTGTGGAGGATTAGAAAAATAAACAGGCAGGAGTCAGACAGTCCTGGATTCAAATCCCACT<br />
TCTAGGCCTTAGAGAAATAATATAATAGTAGGGGATAATAATATTCACCCTGAAGAGTGCTGTAGGGATC<br />
ATCAATATTTCATATAAAGCATGTCATATGGGCAGTGCTCAATGAATGGCAATGCTTTTGCCCAGGTATA<br />
GAACTTCTTAGTATAAAAGTTTTGTCTTTCAGAAAATTAACAAAGATATTCAGGACCGGAATTCAGCTCT<br />
GGATCAAGTAGACCTGATAGATATCTACAGAACTTTCTATCCCAAAACAACAGAATGTACATTTTTCTCA<br />
TTGCCACATGTCACTTACTCTAAAATCGATCACATAATCGGAAGTAAAACACTCCTCAGTAAATGCAAAA<br />
GAACTGAAATCATAACAAACAGTCTCTCAGACCACAGTGCAATTAAATTAGAATTCAAGATTAGGAAATT<br />
CAGTCAAAACCACACAACTACATGGAAATTGAACAACCTTTTCCAGAATGACTCTTGGGTAAATAATGAA<br />
ATTAAGGCAGAAATCAAGAAGTTCTTTGAAACTAATGAGAAAAAGAGAGAATGTACCAGAATCTCTGGGA<br />
CGCAGCTAAAGTAGTGTTAAGAGGGAAATTTATAGCACTAAATGCCCACATCAAACAGCTGGACAGAGCT<br />
CAAGTTGATAACCTAACATCTTAACTAAAAGAACTTAGAGAACCAAGAGCAAATAAACCCCAAAGCTAGC<br />
AGAAGATAAGAAATAACCAAGATCAGAGCTGAACTGAAGGAGATAGAGACACAAAAAATCCTTAAAAAAA<br />
TCAACGAATCCAGGAGCTGTTTTTTGAAAAAATTAATAAAATAGACAACTAGCTAGACTAACAAATAAGA<br />
AAAGAGAGAAGAGTCAAATAAACACAATGAAAAATGATAAGGGGGATAGTACCGCTGACCCCATAGAAAT<br />
ACAAACAACCATCAGAGAATACTATGAACACCTCTATGCAAATAAACTAGAAAATGTAGAAAAAATGGAT<br />
AAATTTCTGGACACATATACCCTCCCAAGACTGAGCCAGGAAGAAATTGAATCCCTGAATAGACCAATAA<br />
CAAGTTCTGAAATTGAGGCAGTAATAAAAAACTTACCAACCAAAAAGAGCCCAGGACCAGATGGATTCAC<br />
AGCTGAATTCTACCAGAGTATAAAGAAGAGCTGGTACAATGTCTGCTAAAATTATTCCAAATAATTGAAA<br />
AGGAGAGACTCCTCCCTAACTAATTCTATGAGGCCAGCATCATCTGATACCAAAACCTGGCAGAGATACC<br />
</dnaseq><br />
<br />
==Labs working on this lncRNA==<br />
<br />
==References==</div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=ZEBTR&diff=1276468ZEBTR2019-08-13T01:47:19Z<p>Qianpeng Li: </p>
<hr />
<div>''ZEBTR'', a lncRNA, promotes the proliferation and invasion of pancreatic cancer cells.<br />
<br />
==Annotated Information==<br />
<br />
===Name===<br />
[[File:ZEBTR1.png|right|thumb|300px|Knockdown of ''ZEBTR'' inhibited proliferation, colony formation, migration, and invasion of Pancreatic cancer cells<ref name="ref1" />.]]<br />
[[File:ZNBTR2.png|right|thumb|300px|The expression profile, cellular location, and distribution of ''ZEBTR''<ref name="ref1" />.]]<br />
Approved symbol: ''ZEBTR''<br />
<br />
Approved name: ''ZEBTR'' : ZEB1 transcriptional regulator RNA <br />
<br />
HGNC ID: HGNC: 53967<br />
<br />
Alias symbols: LncRNA-BX111<br />
<br />
Entrez Gene: 113391337<br />
<br />
===Characteristics===<br />
<br />
<br />
===Function===<br />
* ''ZEBTR'' promotes the proliferation and invasion of pancreatic cancer cells. Mechanically, BX111 activated transcription of ZEB1, a key regulator for epithelia-mesenchymal transition (EMT), via recruiting transcriptional factor Y-box protein (YB1) to its promoter region<ref name="ref1" />.<br />
<br />
* In addition, ''ZEBTR'' contributes to the hypoxia-induced EMT of pancreatic cells by regulating expression of ZEB1 and its downstream proteins E-cadherin and MMP2<ref name="ref1" />.<br />
<br />
===Regulation===<br />
<br />
''ZEBTR'' transcription is induced by hypoxia-inducible factor (HIF-1α) in response to hypoxia<ref name="ref1" />.<br />
<br />
===Diseases===<br />
<br />
Pancreatic cancer <ref name="ref1" />. <br />
<br />
===Expression===<br />
<br />
''ZEBTR'' is overexpressed in human Pancreatic cancer<ref name="ref1" />.<br />
<br />
===Evolution===<br />
===Sequence===<br />
>BX111887.1 BX111887 Soares_testis_NHT Homo sapiens cDNA clone IMAGp998N224461; IMAGE:1755477 5', mRNA sequence<br />
<dnaseq>GCGCCCCACCCCGAAGCCCGGGCTGCGAGGCGGAGTCAGGGCCCCCTCAGCTCCACCCCGAAGCTTGGCATGATTTGCCATTTTACTGCTCCTCTGGAATCTGTGCTTCCTCCCGAGCGCAGGAGGTTCCCCTGCCGCGGCTGCCGGCCCCAGGACCTGGATGGAGATCGCCCGAGGAGAATCCGTTCTCCTGGTCACACTACAGAGGCC<br />
TAGGGGGACGAGACCTGCGGGGCCTGTCCGGACCCGAGGCGGCGCTCGGGATGGTCTCCCGTGGAGCAGA<br />
AACGCCGTTTCCTGGTATTTACAACCCTCCCGACTCCCGGGGAGAGGGCGGCATAGGCAGCCAATCAGGA<br />
TGCAGTCGTCTCTAAAGGTCAGGGTGACACACATTTCCCAAGATCATTCACGGACTTCGCCCTTCGATGC<br />
CTTGTTCTCATGACAAAACCTGGCTGCCAGCACTTAATGTGATTTCCCCCCATCTCTGGCAACTGAGAGA<br />
ATAAAAAACT</dnaseq><br />
<br />
==Labs working on this lncRNA==<br />
<br />
* Department of Pancreatic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Shi-jiang Deng, Heng-yu Chen, Zeng Ye, Shi-chang Deng, Shuai Zhu, Zhu Zeng, Chi He, Ming-liang Liu, Kang Huang1, Jian-xin Zhong, Feng-yu Xu, Qiang Li1, Yang Liu1, Chun-you Wang and Gang Zhao. Hypoxia-induced LncRNA-BX111 promotes metastasis and progression of pancreatic cancer through regulating ZEB1 transcription. Oncogene. 2018 Nov;37(44):5811-5828.<br />
</ref>(1)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=BMNCR&diff=1276467BMNCR2019-08-13T01:46:34Z<p>Qianpeng Li: </p>
<hr />
<div>''BMNCR'', a lncRNA that involves in the regulation of osteogenic and adipogenic.<br />
==Annotated Information==<br />
===Name===<br />
Approved symbol: ''BMNCR''<br />
<br />
Approved name: ''BMNCR'': bone marrow associated non-coding RNA<br />
<br />
HGNC ID: HGNC: 54188<br />
<br />
Entrez Gene: 107985249 <br />
<br />
RefSeq ID: XR_001738390<br />
===Characteristics===<br />
<br />
===Function===<br />
<br />
* ''BMNCR'' regulates the osteogenic niche of BMSCs by maintaining extracellular matrix protein fibromodulin (FMOD) and activation of the BMP2 pathway. ''BMNCR'' affected local 3D chromatin structure and transcription of Fmod<ref name="ref1" />.<br />
<br />
[[File:BMNCR1.png|right|thumb|400px|''BMNCR'' regulated Fmod transcription and local 3D chromatin structure<ref name="ref1" />.]]<br />
<br />
* ''BMNCR'' would serve as a scaffold to facilitate the interaction of TAZ and ABL, and thus facilitate the assembly of the TAZ and RUNX2/PPARG transcriptional complex, promoting osteogenesis and inhibiting adipogenesis<ref name="ref1" />.<br />
<br />
===Regulation===<br />
In human BMSCs, buthionine-sulfoximine (BSO) downregulates ''BMNCR'' expression in a dosage-dependent manner, indicating that elevated oxidative stress at least partially contributes to the reduced ''BMNCR'' expression during aging<ref name="ref1" />.<br />
===Diseases===<br />
<br />
===Expression===<br />
A high level of ''BMNCR'' was detected in the femur and white adipocyte tissue (WAT) in mice. Furthermore, Bone marrow mesenchymal stem cells (BMSCs) and osteoblasts show a higher level of ''BMNCR'' expression relative to monocytes and preosteoclasts.<ref name="ref1" />.<br />
<br />
===Evolution===<br />
<br />
===Sequence===<br />
>XR_001738390.2 PREDICTED: Homo sapiens bone marrow associated non-coding RNA (BMNCR), ncRNA<br />
<dnaseq>TTTTCCTTGATTCCCAGAGTTTCCCTTGTTCTAAATGTACTGCATGAGCTTCTGAATGTACTTGGAGATTTACCAGTACCTCTCCTTGCCAGTTGTAGCTCCTCACCCCAGCCTGTCATCTGTCTGCCCCACCCTCCTCAACCTCTGGACTATAAGAACTCTGAGCCTTGACTTAGTTGTCTCTGTATTCTTAGCTTGCGGCAGTGTCTG<br />
ACACATAGTAGATGCTGAATAAATGTCTGCTGGGAGAATGCATGAATGAATGAATGCATGGAGGAAGAGG<br />
AAGGAGAGGAAGAGAGAGAAGAAGATAGTGGGAAGGAAGAGAGGAAGAGGAAATAAAAAACAGGAAAAGG<br />
AGATGGAAGAAGAAGGAGAGTGCAGTATAGGGTCGGAAAGAAAAAAGGCATCCCTTGATTTGATCTTATC<br />
CCCTTTGTCTTCCTGGGGACTGGAAGGCCCTTCTCAGTTCCTTTCTTTTCCCTCTCCTCCCAACAGGATA<br />
AGGACTTTGGCCACAGCCCTGCCTATCCCCCAGGTATCCCCATAAAGTCTTTAACCCTTAGATATAGAAC<br />
TGCTCTGTCCCTTTTCTACAAAACAAATGTGTTATTTGGGCAGAAGAGGAAAGGAGAAAATTTGAAGTGG<br />
AAAAATCTTTGGTTTGGAAATTCAGCTGACTGCCCTCATTTGGAATAAAATGTCCTTCAGTCCCTGGCTG<br />
TGTGGCAGGCAGGCCCGGCCAACAGCAACACCGGATGCCGGGAGACTGGGAGGAGGCCTGGGGATTTTCA<br />
GAGGAGCCGCCAGAGTGGTATGAACTTGGAATCCAGGAAGAGAGTGATGGGGCTCATCTCCAAGGGCTGA<br />
ATCCCTATCCTCTTCCTCATCTCTGTCCAGACAGTGGTCAGTTGTCCCGATGTGTCAGGCAGAGTGCTGT<br />
CCTGGGGGCACAGACAGGACCAGGAGAAGCAAGTCCTGAGGGAGAACAGGGGCTGGGTCTGTCTCATGTC<br />
CTGAGCACCAACCTCAGCATCTGACACATGGAAGGTACCCAAGAAACATCAGCTGGGAAAAAAAAAGTAA<br />
CCCTTGTCCCGAGGGGTTGACAGGAGACCCAGACTTTGCACTCAGGAGAGAGGGAGGTTGGAAGCGCCAC<br />
TGAGAGGAGTCAGAGGAAAGTGTAAGGAGACTTGTAAAAAAAGGAGGTGGTCATGAGGATGAAAGTCATA<br />
TGTGAAGGATGATGGAACAGAGGGACTAAAGGAGCCTGCCCTGGACACCCTGATTTCCTGCTATGGGGAG<br />
TGAAAAAGAAGCCATAGTCCCATGGATTCTGTTACCAGCCACTGAGTGCAATCCTACCTGATCCCATGGT<br />
CCTCACCAAGGCTGTGTCTGCTTAGGAAATGGAGAATGGTCCCCAAACCACAGCAGCAAAAATGAGTGGA<br />
AGGGTTGAGCATTATTTCCAGCCTTGGTTGCTCTGGTGATTGGTGCCTGGGAGGGGCAGGACCTCCATCC<br />
AACAGACTGTACCAGCAGAGTCGTAAGAGGTAGGACTTTGGAGATTCAGCCGTATGTTCTATGGGTGGAC<br />
TGAAGGCTGAAGGAGGAAGAGGTAGAAGTGCATTGCTACCGACCTACTCCATCCCACGTGCAGACTCCCT<br />
CGACCCCCAACCCCAGGCTGTCACCTGCTCCTATATTCATTTTCTCTGAGGTTGGAGGAAAGAGAAAGGA<br />
GACAGCAATGGCCAGACTTCCCTGGGGTTCCCAAACTGGTTAGTGTGCTCTGCTCAAGTGCTGGCTCCCC<br />
GCCCCTCTCTATGCACACACTCAGCCCATGTTCACTGATTCCCATCCTACCCTCCAGTCATTTGCCTAAC<br />
TGACTTTTTTTTTTCCAGGAAACCTCAGAGATGCATTGGACTTGGTCAGCAGACTTGAGTTCTATGCCCA<br />
TGCCAGTCACTGACTGGCCATGACCTGAGTTGGACAAATCATGCCCACTCTAGACTTAAGTTGTTCCTTA<br />
TATGGAAAAGGAAAGGAGTGCTTTGTCAGTGGTTCCCAGATACCAATTTATAAAGATTTCACTAGTCTGT<br />
GGCAAAATAATATAACAATGGCTATGAATTACTGGGTATTTCCTTTGTGTGAAGTGGTTTTCATATATTA<br />
ACTCATTTAATCTCATAACCACCTGGAAAAGTATGTATTCTTATTAACACCTTCACATGATAGATGATAA<br />
AACCAAGGCTCAGAGAGGTTAAGTAACTTACCTGAAGGTCTTCATATGGTAAGTGGTAGAGCCTGGATTT<br />
GAACTCAGGTATCCTGGTCCCAGAGTCCACGTACTAAATCACTACATTACAGCTACCCATGTGATAAGGA<br />
AAAAGTAAGG</dnaseq><br />
<br />
==Labs working on this lncRNA==<br />
* Department of Endocrinology, Endocrinology Research Center, Xiangya Hospital of Central South University, Changsha, Hunan, China.<br />
* Key Laboratory of Organ Injury, Aging and Regenerative Medicine of Hunan Province, Hunan, China.<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Chang-Jun Li, Ye Xiao, Mi Yang, Tian Su, Xi Sun, Qi Guo, Yan Huang, and Xiang-Hang Luo. Long noncoding RNA Bmncr regulates mesenchymal stem cell fate during skeletal aging. J Clin Invest. 2018 Dec 3;128(12):5251-5266.<br />
</ref>(1)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=LINC02631&diff=1276466LINC026312019-08-13T01:45:48Z<p>Qianpeng Li: </p>
<hr />
<div>''LINC02631'', a lncRNA that might be associated with Compounds containing hexavalent chromium [Cr(VI)] exposure<ref name="ref1" />.<br />
==Annotated Information==<br />
===Name===<br />
Approved symbol: ''LINC02631''<br />
<br />
Approved name: long intergenic non-protein coding RNA 2631<br />
<br />
Alias symbols: AC092620.3<br />
<br />
HGNC ID: HGNC: 54112<br />
<br />
Ensembl ID: ENSG00000237772<br />
<br />
NCBI Gene: 114515520<br />
<br />
===Characteristics===<br />
<br />
''LINC02631'' was nonlinearly decreasing with the change of the DNA content of comet tails (Tail DNA), tail length (TLL), tail moment (TM) and Olive Tail Moment (OTM), and the fitting results of Tail DNA and TM were statistically significant (P <0.05)<ref name="ref1" />.<br />
<br />
With the increase of Cr(VI) concentration, the expression of ''LINC02631'' increased gradually, indicating that ''LINC02631'' was likely to be candidate biomarkers for Cr(VI) exposure and DNA damage<ref name="ref1" />.<br />
===Function===<br />
<br />
===Regulation===<br />
<br />
===Diseases===<br />
<br />
<br />
===Expression===<br />
Compared with the control group,''LINC02631'' was significantly up-regulated with increasing concentrations of Cr(VI) (P < 0.05)<ref name="ref1" />.<br />
===Evolution===<br />
<br />
===Sequence===<br />
<dnaseq></dnaseq><br />
==Labs working on this lncRNA==<br />
* Department of Occupational and Environmental Health Sciences, School of Public Health, Peking University, Beijing, China.<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Hu G, Feng H, Long C, et al. LncRNA expression profiling and its relationship with DNA damage in Cr(VI)-treated 16HBE cells[J]. Science of The Total Environment, 2019, 655:622-632.<br />
</ref>(1)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=UMLILO&diff=1276465UMLILO2019-08-13T01:44:53Z<p>Qianpeng Li: </p>
<hr />
<div>''UMLILO'' is a prototypical immune gene–priming lncRNA.<br />
<br />
==Annotated Information==<br />
===Name===<br />
Approved symbol: ''UMLILO''<br />
<br />
Approved name: ''UMLILO'': upstream master lncRNA of the inflammatory chemokine locus<br />
<br />
HGNC ID: HGNC:51824<br />
<br />
Ensembl ID: ENSG00000228277<br />
<br />
===Characteristics===<br />
''UMLILO'' is a multi-exonic 575–base pair(bp) lncRNA and is transcribed from within the chemokine superenhancer<ref name="ref1" />.<br />
<br />
===Function===<br />
<br />
* ''UMLILO'' acts in cis to direct the WDR5–mixed lineage leukemia protein 1(MLL1) complex across the chemokine promoters (IL-8, CXCL1, CXCL2, and CXCL3) facilitating their H3K4me3 epigenetic priming<ref name="ref1" />.<br />
* ''UMLILO'' is a cis-acting lncRNA, playing a key role in the expression of chemokine genes. ''UMLILO'' is central to the deposition of H3K4me3 on chemokine promoters during trained immune responses, and the deletion of UMLILO abrogates chemokine transcription<ref name="ref1" />.<br />
<br />
===Regulation===<br />
It is reported that β -glucan-mediated NFAT signaling increases immune gene–priming lncRNA transcription, including ''UMLILO''<ref name="ref1" />.<br />
===Diseases===<br />
<br />
<br />
===Expression===<br />
CAGE data showed that ''UMLILO'' is unidirectionally transcribed and expressed in innate immune/non-immune cells(monocytes, endothelium)<ref name="ref1" />.<br />
<br />
===Evolution===<br />
<br />
===Sequence===<br />
>4 dna:chromosome chromosome:GRCh38:4:73709702:73715127:1<br />
<dnaseq>TTTTGTGACCAGTGTCCTGAGCAATTGGCTTCATCTAGGCCTCAGATCACAAAACAGAGT<br />
TGTATAAAATGGAAAGTGCAATGCTTTTTTAGTAAAATAACTTTTCTCTTCCTTCCTTTC<br />
TTGCTTTTTTCCTTCCTTCCTTCCTCCCTCCCTCCCTCTCTTCCTTCCTTCCTTCCTTCT<br />
TTCCTTCCCCCACTTTTTTTTTGGCAGGGGGATAGAATGTAAGACTATATATATCAGATA<br />
ATTCTCTGGGCTACATTTTAAAATTTTCATCTGATAATTTACTTTTGTTTCTGTGTGGTA<br />
GGAGTGAGAGCTCTCAATTATTTAGCACTAATTGTGTGCCAGGTTCCATCTGAAGGCTTG<br />
ACAAGAGTCACCTTAATTCTTTGCCATATTTTGAGGTAGATACTACTGGCACCATTTTTT<br />
AGACTGAGAAAGGAGATGTAGAAAGGATAAGATGTTGTCCAAATCCACATTGACAGTAAG<br />
TTTTGGACATGAGTCTTTAATCTAGCAATATCCGACTTTAGAGTGTGTTCTTAAGCACTA<br />
CTCTATAAGTTTTAAGCAGCTCCTTTATGATGTCATTGAACCGGGTTTTCCAGTCACATT<br />
ATACATGTGGAGATTAAGACCCATAATAACAATGACAACACTTTCATAACAGTTCATCTG<br />
TGTTAACATACAAATTCTCGCAGCAACACTCCAGGTAAGTGCTCTTTTTATCTCAGTTTT<br />
ATGGATTAGTAACTGAATGCAGAGAGGTTAAGCAACTTGTCCAAGATCACATAGGAGTAG<br />
GTAGTAGAATTGGGATTTAAAGCCACACTCTTAACCACAATTCTACTCTGTCCCTCTGAG<br />
TTATAAATTTAATTAGTATGACATAAATATATGTGCAGCTCTTTTAAAGATTTACTGTGC<br />
ATATTTTTAAAATTGTTACAACATAAGCATTCTAGGCTTTTATTAGTCCTCCAACTTTAA<br />
CATTTATGCTTTCATTTTTATCTTGTAAAGTCTTAATTTATAATAAAAAATGGATGTGTA<br />
CTGTCCCATATGTCTTCTTTATTTATTTATTTATTTATTTATTTGAGATGGATTCTCCCT<br />
CTGTTGCCCTGGCTGGAGTGCAGTGGTGCCATCTTGGCTCACTACAACCTCTGCCTCCTG<br />
GGTTCAATCGATTCTCCCACCTCAGCCTCCCAAGTAGCTAGGATTACAGGCTCCCACCAC<br />
CAGGCCCAGCTAATTTTTTTGTATTTTTGGTAGAGACAGGCTTTCACCATATTGGCCAGG<br />
TTGGTCTTGAACTCCTGACCTCATGTGATCCGCCTGCCTTGGCCTCCCAAAGTCCTGGGA<br />
TTACAGGTGTGAGCCACTGCACTGGCCCCGTATAAAGAGGAAGATTTTCCAAACACTGAT<br />
GAAACCTCTAACAACATACTCTGCAGTTCATAGATCGTTCCTACCTAGAATTTAATTCGT<br />
ATATGCATACTGTTTCTTCAAAGCATTAAGAATGTGCAAACAAGACTTCTTGGAAAAATG<br />
AGGCATATGGCATGCACAGTCATGAGCTTCATGGCAGGAGGGCAAGGGGAACACTAAGTC<br />
ACTTGGGGCCATGAGAAAGGAACTCTGGTCCTGTCCTGTCCTTTCCCAGAGCAGGGATCC<br />
TAACACTTCTAAGAGAAGGGCCATTGGTAGCCTCTAGTTCTCAGAACTGTTTGTCCGCTA<br />
ATGAAAATTAACACACTTGATTTTGGACAGGTTAATGTGAGATATCTATTATTTCCCCAG<br />
TGAGATATCATGTTGGCAGTTGGATATATTCAAGTCTTGAGTCAGTTGATACCGACTAGA<br />
TAGATAGATACATAAATACATACATACATAGAAAATATTAACAGCAAAATGATGCTGATG<br />
GCTCAGGATGTGTGTTGAGACAGACAGAACTGGGTTTTGTCATTCAAGCCGTTATTCACA<br />
CCCAGTGTCACCTAGGCCAAGGTTTGAGCTGCAATTACTTCAACTGTGAAATGAGGTTTC<br />
CTTCAACAGATATATATTGAATGCCTAGAATGTTCCAAGCACTGTTCTAGGTACTGCATA<br />
GAGCAGTGAAAAAAAAAAAAAACCTGACAAAATCTTCGCCCTTCTTAAGTTTATATTCTA<br />
GTGTGTGTGTAGGAAGGAGGGGAACATGGAAAGTCAGGTACTAAATTGGTGAAAAGGGAA<br />
AATATATAGTATGTCAGATGCTTACAAGTATTAAAGAATAAAATAATGCAGAGAAGGTGA<br />
AAGGAAGTATTTGCTGCAGGAAGAGATGAGGAGCTGAAGATGGTGAGAGTTAGAATTGTA<br />
AATAGGACAGTCAAAAAAACCTTCACAGAGAAGCAAAAATTCTAAGGCAGGAGAGGGAGG<br />
GAGTCAGGTAGCTATCTGAGAGAAGACTGTTTCAGCAGATGGAAACAGTCTTCAACAGAG<br />
GAAAGAGCTATTGCAAAGACTCAACGCCTTGTGAGATAAAGGGAAAAAAATCAATGTAGC<br />
TGAAACAGACTGAATGGAAATCAAGAGGCCATAGAAACCACAGAGGGGTTGAAGATGTCA<br />
CTGCAGTTTTAGGCTGAGAGACTGGAAAGATGGAGCTACTGATTACTGAAATGGAAAACT<br />
CTTTGGGAGGAGTATATAATTTTGGACAAGTTAAGTTTGAGATTTCTATTGCTGCCCAAG<br />
CGAGTTGTCAAGGAGCCATTTGGATAGTCATATCTGGAGTCAGCAAAGGAGACCAGGCTG<br />
TACATACACATGTGCAAATTGTCAGCTTTTGAGGATATTTATAGCCACAAAAAGTGGGGA<br />
TAGGTAGAGAAGGAAAGAGGTCTCAGTTCCAAGGGATTGGAGTTGGCTACTGTTTAGAAA<br />
TCTAGGAGGAACCAGCAACAGAATGACAGAGAAACCAGCAACAGGGTGGTAGAGAAAATT<br />
CAGGAATGTGTAGTATCCTGGAAGCCAAAGGAAGAGGAAGAGAAAGTAAGCTTCTACGTG<br />
AAATGTTGCAGATAAGCTACTTTCTTCACAGCATTACTGCATGAGTTAAATAAAATGCTA<br />
TTTGTACAAAACAGCATAATATCTGGCACAGCACTGCAGGTAAAGCTTGTTTTCATTTTC<br />
TACAATGAAGTTTTAAATGAATATTTAAAAATATATTTTGGACTTCTCAAAGCAAAATGT<br />
AATCCCATTTATAATTTCATAAAGACATTTTATCTGCTAATATCAGGACATCATTTTCTC<br />
AAACACAATGAAACTTTTTAAATGTGAGAAAATAAAATACTTCTCAGAGGTATTTCATAA<br />
AAGCTTAAGATAGACTCTTTTTGCCTCATAACTTTTATGTATAATTTAATAAAAGGTAGT<br />
AATGAGAAAATCAGATCTAATATATAGAATTTTGTTTCATAACCAAATTTTTAGAAATAA<br />
GTCATCTTATATATTAAAGAATAGCTAGAAGGAGAGAGGGATGAATTTTATGTATAAAAT<br />
TTATGTATAATAATTTTTCCTTATAAAATTTATGTATAATTTTATAAAAGGTAATAATGA<br />
GAAAATCAGATCTAATACATAGAATTTTGTTGCATAATCAAATTTTTAGAAATAAATTAT<br />
CTTATATATTAAAGGATAGCTAGAAGGAGAGAGGGATGATGAAAGGAAAAGAACAAGACA<br />
TTTTTCATGCTTACTCTGTGTGACACGCTCTGCAGGGCGCTTTATGTGTGGATCTTTTTT<br />
AGTCTGCATATTAACCCTACAAGTTGGAAATGGCTCCTCTCAAACACTGGAGATAGAGCA<br />
GCCCAAATGTATCTGCTACTGTGGTGCCTTCCATGTGAGTATTTTCTCCAAATGCTAATT<br />
TGGAGAAAACAATTTATATGAACGGAGACACTATTACTTATTTGCCCTCAAAAATGAAAG<br />
TGACCCAAGGCTGGAGATAGGAATTTGTCCCAAACAATGTCTTCAGCCACCCCTCCAAAC<br />
AAAGTTTGAAAGGGATGTGAATAAGTAAATGCAGAATCAGAATTTTCTATCTCTTCTGGC<br />
CTAAGTTCTTCATTTCTTAGTTGAAGATAACCAAGGCCAAATCACGTAATCAAATGACAG<br />
AAAATTATTCTGGAGACACAACCAGGCATATCAGATCTGTCTGTTTTTGGCTTGTGATGT<br />
CCACACACAACACCTGTGAACAGGTGCACTCAGCCTACCAGGAAATGCACTCATCATGTG<br />
TCATCTACAGATTTTCTCAAGACTAGAGCATTTGTGAGAAATGACCGTAAGGCTTTCCCT<br />
GTGGAGTTGAATACAAAGATTGAACATAGACATTTTGAATAATCCTAGTGACTTGCGGAT<br />
CCAGTTTCCATAGAGCACTAGTTTCTCTAAGGCCACAGTCACTAAATGAGGTTCCATGGC<br />
AGGTGTAAAATCTCACTGGGTGATTGTGTCATGCTGTGCTTACAGCACTATGTTGGGGGA<br />
GAAGAGAGGAAAACCTATTATTGAAATCTGTGCTATTTTACATGACCTTTTAATTACTTA<br />
TTTTTAAAACATCTCTCCTTCTAGAATGCAAAACTCTCTGAGGAGCTGAGAATATGTCTA<br />
CTGCTACCAAAATTGTAACCCCCATCATCTAGTAAAGAGTTGGTACACGGTGAACATTTG<br />
CTGTGGGAATGTATTCTGCTTCATTCCAGAGGCCTGCCAATTCTTAATCTCACTATAGGC<br />
TGAAGAGCTGCTCACATAGAATACTTGTAGTGACTTCCATTTTCACCAGTTTAGATCAGT<br />
GGACAGAGAGATGCTGAATTACTGCTCAAGAAGTATAGATCCACATGCCTTCAACTTCAG<br />
AATCTTAAATTAGAGGCGAATGTTGAGTCTACTAAACTGTATAGTCTGTAAAGGCAGGAA<br />
CTGTATTTATCTCAGTCATATTTAATCCCAAGAGTCTTCATAGTACCTGGCCCATATCCG<br />
TTGTTCAATAATTGGTTTTTTAAATACCTAACTTATTAAACAATGTGTTTGATTAAACAG<br />
CAGTGACAAAAAAGGGCTTACTCAGTCTTAAGTGCTAGAAGTAAAGACAGTCATGAGGGG<br />
CTTGCAATGAGCTCCACTGGGGGGAATTTTTCTTCTTCACATTTTTGTACAATGAATGTC<br />
ATCACAGGACACAGCAGATACCCAAGAAATATTATTTTAAGGTATACTATACTCAAAGAA<br />
AACCAGGAAAGCCAAAAGACTCTTAATTAATAGAAAACTGCTGAGTCAATAGGATAGCTC<br />
ATATAAATAAATTGTGTTCAGAATTTGATTTTCTAAATTAAAAAAAATTATGTAGTAATA<br />
TCTCGAGTATAACAAATGTTTTAAGAATGGATTTGTGAAACTACGGCCATTTAAATAATA<br />
TCTTGAAATGTTCAAATATCAAATCTTTATTGAATTATATTCTACATAGTGATTAATCAA<br />
AAACTAAACTAGATCTTAATTCTCACTGTAGAAAGTAAGTAGTCTTATAATATATTTGTA<br />
AAATTAACATTTTAATGTTTAATTAT</dnaseq><br />
<br />
==Labs working on this lncRNA==<br />
* Gene Expression and Biophysics Group, Division of Chemical, Systems and Synthetic Biology, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Fanucchi S, Fok ET, Dalla E, Shibayama Y, Börner K, Chang EY, Stoychev S, Imakaev M, Grimm D, Wang KC, Li G, Sung WK, Mhlanga MM. Immune genes are primed for robust transcription by proximal long noncoding RNAs located in nuclear compartments. Nat Genet. 2019 Jan;51(1):138-150.<br />
</ref>(1)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=PCED1B-AS1&diff=1276406PCED1B-AS12019-08-12T04:08:56Z<p>Qianpeng Li: </p>
<hr />
<div>''PCED1B-AS1'', a long noncoding RNA, is involved in the regulation of macrophage apoptosis and autophagy in active tuberculosis.<br />
<br />
==Annotated Information==<br />
===Name===<br />
Approved symbol: ''PCED1B-AS1''<br />
<br />
Approved name: ''PCED1B-AS1'': PCED1B antisense RNA 1<br />
<br />
HGNC ID: HGNC:44166<br />
<br />
RefSeq ID: NR_026544<br />
<br />
===Characteristics===<br />
<br />
===Function===<br />
<br />
* ''PCED1B-AS1'' modulates macrophage apoptosis and autophagy by targeting the miR-155 axis in active tuberculosis (TB)<ref name="ref1" />.<br />
<br />
===Regulation===<br />
Since ''PCED1B-AS1'' modulates macrophage apoptosis and autophagy in a ceRNA manner, miR-155-targeted genes play vital roles in PCED1B-AS1-meditated macrophage apoptosis and autophagy <ref name="ref1" />.<br />
===Diseases===<br />
Tuberculosis<ref name="ref1" />. <br />
<br />
===Expression===<br />
''PCED1B-AS1'' is down-regulated in monocytes from patients with active TB<ref name="ref1" />.<br />
<br />
===Evolution===<br />
-<br />
===Sequence===<br />
>NR_026544.1 Homo sapiens PCED1B antisense RNA 1 (PCED1B-AS1), long non-coding RNA<br />
<dnaseq>GGAAGCGGAAGACTAATGACCGAAGCTTCAAGACTTTGACATGTGTGAAAACATGAAATGACCCTTGGCT<br />
CTTATTGTTCTTGCTGGTGTGGTATGTTCACGGCTGAAAAGATGGTCAGAAGGGGAAAGGAGGAAGTGAG<br />
AAGAAAGAAACAGGGAAATGACAGAGTGTTGCTCAGTTACCCAGGCTGGAGTGCAATGGCATGATCTTGG<br />
CTCACTGCAGCCTCCACCTCCTGGGTTCAAGCGGTTCTCGTGCCTCAGTCTCCCAAGTAGCTGGGATTAC<br />
AGGTATGCACCACCATGCCCAGCCAATTTTGTATTTTTAGTAGAGGCAGGGTTTCACCATGTTGGCTAAG<br />
CTGGTCTTGAACTCCTGACCTCAGGTGATCTACCTGCTTCAGCCTCTCAGAGTGCTGGGATTACAGGCAT<br />
GAGCCACCAAGCCCGGCCTGAAATACATTTAAATAAATGAAGATGGAGAATCAGACATTACTTTCATTTA<br />
TCTGAATCTGGTGTAGTTTAATTAATCTGTAATTGTAAGTCTTTGAATCATATGTCAATATTCTATTTTG<br />
TTAGTCATGATTTCTAAGTGTTACATAACTGTGGCCCCAGCCACTTTATATTTTGGTATCATGACAGAAG<br />
ACTCTGATTGTGGTTATTTTCTACCTATGCATTTATTCTTAGTGATATATGTTGGTTAAATTATGGCATA<br />
GTTTTAAAATACATGACAAAAATAGCTAACAGTAAAGAAATGTCTTTGTTTCTGGTTGAATAAACTGACC<br />
ACGCAAGGTTCCAATTTAAAATAAATTCTAAACGAATCATGTTATTTTCCAAAACTGTTCCTCCTCTCAG<br />
TAAATGAAATCAATATCCACCCGGTTACCCCAAGACAGAAATCTCAAGATCATCTGTGACTCCTTCCTCT<br />
TCATCTGCCACAAGAAGAGTAGCTTCTATCTCCAAAGCTAGTCTCTGATCAGTCTACTTCTCTTCCTATA<br />
GCCTCTGCTTTAGTTCAAATCTAGAATCCTGCTGTGGTGGTGCTGTGGCTTCCAAGTTCATCTTCTTCCA<br />
ATCCGTTCTCTAAACTACAGTCTTGCTCTTTCTAAGACTCAGATCTTATAATTTTACTTCCCTTCATAGG<br />
TTGAATTTAACCTGCTAAATCACATAAAATTTTTCTGAAGATACCAGCCTTTCTGCCTTAATCAAACACA<br />
TTAGCCAAATCCATAGCATTACTGGGATAAAGCCTGAAGATCCCAAATTGATAAGGCATCTGGATTCCCT<br />
TTGATAACAGTATTCAATAACAATGAACACCTACTGAGTATACTATTCCAAGCATTTAAAGTGTATCAAC<br />
TCTTTTCACAAAATCAACAATAATTATTATTGCTACCATTTATTGAGAGTCTACTTTAATCCAGGTGTTA<br />
CATATTCATGTATTCATTATTATTACCTTTTTTTTTGAGACGAAATCTTGCTCTGTTGCCCAGGCTGGAG<br />
TGCGATGGCATGATCTTGGCTCACGGCAAACTCCGCCTCCCTGGTTCAAGTGATTCTCCTGCCTCAGCCT<br />
CCCGAGTAGCCGGGATTACAGGCATGTGCCACCATGCCCCGTTGGCCAGGCTGGTCTCGAACACCTTACC<br />
TCAGGTGATCCTCCCACCTTTGGGATTACAGGTGAGCCCAGCCTATTGTTACCTTTAAAACCACCCTGCA<br />
GGGTAGCTCTTACTGTCTCCATGAGGAATATCAGAAAAGGGAAAGGACTTCCTGGAGGGCTGGTTCTGCC<br />
TCAAGCCAATCAGCTGACACTAAGCAGTGAAGCCGGAATCTGAGGTCCCTCTGCCTGCCCTGGTCTTTGC<br />
TCACCCTGACAACCAGACACCTCACTGTGTCCTGAGCAGCATAGATGCCACACGCACAGTGCCACATAGA<br />
GAAGGGTGATGTAAATGAAAATTAAAACACTGTGACAAAGTCAAGCAGGGCATTTGTTTTTGTTGTTGTT<br />
AAGTTATTTTTGGTAGATACAGGGTCTCACTATGTTGACCAGGCTGGTCTTGAACTCCTGGGCTCAAGCA<br />
ATCTGCCTGCCTCAGCCTCTCAGAATGTTGGGATTATAGACATGAACCACTGCACCCGGCCAGTGTCAGT<br />
CTTTGTTCCCTACAAGTGAAATCAAAACAGCCTCACGCCTGTAAACCCAGCAGTTTAGGAGCCCAAGGTG<br />
GAAGGATCGCTTGAGCCCAGGAGTTTGAAACCAGTCTAGGCAACATAGTGAGACCCTATCTATACAAAAA<br />
TAAAAATAGCCTGGGCAGGGTGACTCATGCCTATAATCCCAGTACTTTGGGAGGCCAAGGTGGGTGCATC<br />
ACTTGAGGTCAGGAGTTCGAGACCAGCCTGGCTAACATGGAGAAACCCTGTCTCTATTAAAAATACGCCT<br />
GTAGTCCCAGTTACTCGGGACGCTGAGGCAGGACTGCTTGAACCTGGGAGGTAGAGGTTGCAGTGAGCCG<br />
AGATCGCGATACTGCACTCTAGAGCCTGAGTGACAGAGTGAGACTCCGTCTC</dnaseq><br />
<br />
<br />
==Labs working on this lncRNA==<br />
* Fourth Tuberculosis Internal Medicine Department, The First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan, 453100, PR China<br />
<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Mingying Li, Junwei Cui, Wenyi Niu, Jian Huang, Tianjuan Feng, Bing Sun,<br />
Hengbo Yao. Long non-coding PCED1B-AS1 regulates macrophage apoptosis and autophagy by sponging miR-155 in active tuberculosis. Biochem Biophys Res Commun. 2019 Feb 12;509(3):803-809.<br />
</ref>(1)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=MYOPARR&diff=1276405MYOPARR2019-08-12T04:07:30Z<p>Qianpeng Li: </p>
<hr />
<div>''MYOPARR'', a long noncoding RNA, is essential for the expression of human myogenin gene, which is one of the key myogenic transcription factors.<br />
<br />
==Annotated Information==<br />
===Name===<br />
Approved symbol: ''MYOPARR''<br />
<br />
Approved name: ''MYOPARR'': myogenin promoter-associated myogenic regulatory antisense long non-coding RNA.<br />
<br />
HGNC ID: HGNC: 54178<br />
<br />
RefSeq ID: NR_160550<br />
<br />
<br />
===Characteristics===<br />
''MYOPARR'' contains a potential RNA nuclear retention signal at the 5’-side, a putative polyadenylation signal 15-nt upstream of the poly(A) tail, and a LINE-1-like sequence in the 3’-half<ref name="ref1" />.<br />
===Function===<br />
[[File:functionofMyoparr.png|right|thumb|Proposed model of Myoparr function during myogenesis<ref name="ref1" />.]]<br />
<br />
* ''MYOPARR'' is essential both for the specification of myoblasts by activating neighboring myogenin expression and for myoblast cell cycle withdrawal by activating myogenic microRNA expression. Mechanistically, ''MYOPARR'' interacts with Ddx17, a transcriptional coactivator of MyoD, and regulates the association between Ddx17 and the histone acetyltransferase PCAF<ref name="ref1" />.<br />
* ''MYOPARR'' also promotes skeletal muscle atrophy caused by denervation, and knockdown of ''MYOPARR'' rescues muscle wasting in mice<ref name="ref1" />.<br />
<br />
===Regulation===<br />
<br />
''MYOPARR'' expression is regulated by MyoD and TGF-b. During the conversion of C3H10T1/2 fibroblasts into myogenic cells by MyoD expression, a significant increase in ''MYOPARR'' expression was observed. In contrast, TGF-b treatment significantly decreased Myoparr expression during C2C12 differentiation<ref name="ref1" />.<br />
===Diseases===<br />
<br />
<br />
===Expression===<br />
''MYOPARR'' is co-expressed with myogenin, the expression of which is highly restricted to myogenic tissues in embryonic, fetal, and adult skeletal muscles <ref name="ref1" />.<br />
<br />
===Evolution===<br />
-<br />
===Sequence===<br />
>NR_160550.1 Homo sapiens myogenin promoter associated myogenic regulatory antisense long non coding RNA (MYOPARR), long non-coding RNA<br />
<dnaseq>AGAGCTGGCTTCCTAGCATCAGGGCAGCCTGGCTTAGGAGGCCCCTGCTACAGAAGTAGTGGCATCTGTG<br />
GCCAGCTTGGGGGGCTCGCAAGGATGCCCGGCTTGGAAGACAATCTCAGTTGGGCATGGTTTCATCTGGG<br />
AAGGCCACAGACACATCTTCCACTGTGATGCTGTCCACGATGGAGGTGAGGGAGTGCAGGTTGTGGGCAT<br />
CTGTAGGGTCAGCCGTGAGCAGATGATCTGTAAGGGGAGGTGGGAAGGTGGTACCTGGGTGAGCAGTGGG<br />
GGTTCTTGAGGCCCAGAATAGAGGATGGGACCCTTGGGGTGACAGAGGTTTTCCAGGACAGATGAATGAC<br />
AAAGCTCCGGAGTTCTACTCCCTAGTCCCTGCCTTTCCCCATGCTCTGTGAGTGTGTGTGTGTGTGTGTG<br />
TGTGTGTGTGTGTGTGTGTATGCGCCTCTTTTCTGAACTCCCCTAGTAGGTAGGGTTTGGAAGCAGCCAC<br />
TCAAGTTGGAGCAGGATGGAGCTCCCCAGAGACTGGACCTGCCCTTTGCTCGGCCCAGTTTTGCAGCACT<br />
GACTCAGCACTTCACAGGGACCCCTGGGGCAGGGACATTGTCCTCTCTGTGGAGAAGGTCAACCACCAGG<br />
CATCAGCTGGGGAGCTGCAGGAGCTACTATCACTCCTTTGCTGGTCAAGACTGCAGGGGCACACAGAACC<br />
TCCCAGCCCACCCTTTGGGCCTTGGAGTCAGCAGGTCCCTAGAGAGACCCAAGGGAAGAGGACCGGAGCA<br />
AGGAATAAGGTAAGAGGGGAGAACCTGGCCCAGGGAGGGACTGAGGGATTGGAGCCAAGGTTACCAGTCA<br />
GGCCTTACTTACCCCCTGGGTTGGCGCTGAACTCCAGTGCACTGCCCCACTCTGGACTGCAGGAGGCGCT<br />
GTGAGAGCTGCATTCGCTGGGCACCTGCAAGACAGGGCGAAGGCCCAAGGTCGGGGCACAGCCATTCTTT<br />
GATGTCTCTCTCTGCCTAGTCCCAGTGGGCAGAAGTACCTGTGGTGGGGTTGGAGGGTGGGCCACAGGCT<br />
GTGGCCTTCCAGCCCAGGCCATCCCCAACCCCAGAATCTTTGTAACTAGCTCCTCTCACACCCCAGAGGC<br />
CCTGCTTCCAGGCCTTCCTGGCTTCCATCCTGGGTGGTGGTTCTGCTCTCACAGGACACCAGCTTAAAGG<br />
GGTCCCTGGTTCTCCTGACTCTGGCGATAAGGGTGATGGAGACAGATTTTGTGGCCCAGTGAAGGTCGCT<br />
CTGTGCAGGCCTGCTGGAGTTCCAATGAGACTGAGTGGGTTTTCTCTCTGCTCAGCCACACCCAGGATGG<br />
GGGCAAAGCAGTCTTCTCTGGTGAACTTGGCCTGGCCTTTTAGGCTCTGACTCAGGCGCTGGGATTAATC<br />
CTCACCCTCACCTGGGCTGACTGTGGCCTTGCTCCTGATCTTTCTTCAGTCCTATGTTCCCCACCCCAAC<br />
CCCTTCTGCACTTCCTCCCCACTGCCTTTATCTTGTCTGGAAAGAACACAGGACACAGGAGGTCAGCTGG<br />
ATAGCCCAGCTCTGACCAGGGAAGGGCTCCTGCAGCCCCTCGACCCTGTCTGGCACCTGCACCAACCCTC<br />
TGAGCCCCTCTTGGGGTCTTGAGGCTGTCCAGGTGCCTCCCTCTGGCCCCGTCCCCTTGGGGCAGGGGGA<br />
TGGGATGGCCACTTACCCCTGGCTGGGGCCCGCCCCCGCCCCGGTAGCGGAGGTCACGCTCCTCCTGGTT<br />
GAGGGAGCTGAGCAGGGCCTGGAGGCGCTCGATGTACTGGATGGCACTGCGCAGGATCTCCACCTTGGGC<br />
AGCCGCTGGTTGGGGTTGAGCAGGGTGCTTCTCTTCAGGGCCTCGAAGGCCTCATTCACCTTCTTGAGCC<br />
TGCGCTTCTCCCTCAGTGTGGCCGCCCGCCGCCGGTCCACGGACACCGACTTCCTCTTACACACCTTACA<br />
CGCCCACGGCAGGCACTGGCCTGGACAGTGCTCGGGGGTCCCCAGCCCCTTGTCCTCAAGGGGCCCTGGG<br />
GCCTCGGGGCTCAGGGTGAGCTCCGTCCGCTCGTAGCCTGGTGGTTCGAAGCCCTGGAGGTGGACAGGCA<br />
GGTAGTTTTCCCCATCATAGAAGCGGGGTTCCTGGTAGAAGTAGGGGGATGTCTCATACAGCTCCATGGG<br />
GTCGGAAAAGGCTTGTTCCTGCCACCAGCCCCCAAGCTCCAGCAGCCCCTCACGCCAACTGCTGGGTGCC<br />
ATTTAAACCCTCCCCGCTGGCATGGAACCAGAGATAAATATAGCCAACGCCACAGAAACCTGAGCCCCCT<br />
CTAAGCTGTTGCTGCACATCAAGGCGTTTACAGTGGATTAGATGTGATTCCCCTTCTTTCTCCCGCATGG<br />
CCCCCACCCCACCCTGCCAGCCTGCCCCTGGCCCAGGCGGGCTCCTGTGCACGGGTCGGGAGGCCGTCGG<br />
GTGTAATTTGATTAGTTTTCATTTCTCAGCAGCCCCTGTGGGGCAGGGGCGTTGGGGGAGGACACATTCC<br />
CCTCTCATCTGCTCCTTTCAATTACTCCTAGCTGGGCGGCCTGCCTGCTGTCTCCTTGCAGTCCCGAAGA<br />
AGCTGGTGGGTATAGGGGGAGGAGGGAACAAGGAAGGGTAGGCTTAGGCTGGAAGGGGCCTTAAGAGCCA<br />
ACTTATCCATCTCCTTGCTTCCTGACAGCACCTTAACCACACTACATCAGTCGATGAGACTCTTTTAAAG<br />
ACTTCCCTCCGGAAAGAATGGGACTGCTTCAGATTCTGGGCATTCATGGGCACTCAGTATCCAGGGATAA<br />
GAAGGATCAAGACTCAGAGCAGCTAACAGATTCCACTTTTGGGGTTCCCAAGCAGCTTTGAGCTGTATGT<br />
TCTCTTAGGTCTCATCTGGGGGGGTAAATTGAGGCAAGAGAAATTATTTGGGTTTTGGTTTTCTTGGCAG<br />
GGGTAAAGAGAAATTTCCTCTTTAATACAGCAGCCGTGGTCAGAGCAGAGATTAGAATTTACAGCCTACA<br />
CGTTGCCACCTTCCCCAGAGCGGCAAGGTCAAGATGTCCTAAGCTCCCTGTCTCCTCCCTGTCTCACTCC<br />
GGACCATTGATCTGTCCTTCTATGTTACCTCCTCAACTCTTTTTCCAACACCAGAATTTTCCTGGCTCAT<br />
TAATGTGGACGGGGGTGAAAAAGTAGAAAAAACAGAGCCCTTCAAACTCAGTTTAAATCTCCTCTCTCCT<br />
TGGCCACCGGGCTTGGTTGTTCTGCCTCTTACTGTCTGAGCCATCAATTTTACACGTATCATGCAGGTCT<br />
CAAATGTCAGGTAGAGCAGGGACTATTTAATCTTCAGGCCTCTCAGGCCATGGTCACCTCTCAGTAGGTG<br />
CCTCAGGGTCTGAGAGGACAAATTCCTTCCAATGCAGTGGGCAGACCTTAGACACTAGCAGTGAACAAGG<br />
CTCAGTCTTAGGGCTGGGGATTATAGGGACACCCCAGACAGGATCCCTGCCCTCGAACTTACCATCTGAT<br />
AGACAACGGTGATCACCTCTTTCTACCTAGCCCCTGATGCCCAAATCTCCTCCGAGGCGGCTACTGTTCA<br />
GCTTCTGCTCACGTCAGGAGACAGCCCGTTCCATTGACGTGTAGCTTTGGGCTGCAATCTGCTCCCTCTA<br />
TCTTTTATCCTTTGTTCCCAGTTTTTTCCTCCCCATAGACTAATGTCCTGCTCCTTATCCTACGACAGAT<br />
CAAACTGACAAGTTCAAGCCAGTGGCAAGGACAATAAGAGGAAGGGGAACCCTGCTGGGGACTCATGGGA<br />
GACTTCACAGGGAACATGAGATCTGCGAGGCATGTGAAGAACCAGTGTTCCTTCCTCTCATTATTCACAG<br />
CAGGGAGCCAGGAGAATTCTGATGTCCTTTTGGGACAGGAAATGGAGGGAAGGAGGGAACATAGCTGGAC<br />
AACAAAAGAACCCTAAGCATGTTGAGGGAGAGCAGTGAGGTCTTAATTCTGTTCTTGGCCTTACCAGCAT<br />
GATAGAAAGTAGCAGCATAGGCCGGGCGTGGTGGCTCATGCCTGTAGTCCTAGCACTTTGGGAGGCCAAG<br />
GCGGGTGGATCACGAGGTCAGGAGTTCAAGACCAGCCTGGCCAAGATGGTGAAACCCTGTCTCTACTAAA<br />
AATACAAAAATTAGCCAGGCATGGTGGTGGGCACTGTAATCCCAGCTACTTGGGAGGCTGAGGCAGGGAA<br />
TTACTTGAACTCAGGAGGAGGAGGTTGCAGTGAGCCGAGTTCGCACCACTGTACTCCAGTCTGGGTGACA<br />
CAGCGAGACTCTGCCTCAAAAAAAAAAAAAAAAAAAAAAAAAAAAAGTAGCAGCATAGGTACTGTGTGGG<br />
TTCTAAACTTTGCTTTCCCCTGACCAGCTGGGCTGAAGAAGAGTCTCTATTTCTAACACATCCCCTGCCA<br />
AACAAAAAAGAAAAAAAAAGCCTCAGTTTACCCTCCAGTCCTATGAGCCCTGAGAAAAGAAGTCATGTTG<br />
AAGCCACTATAGGAACCCCCATATTTGCATCTTTTGTTATTCCAGGATCCAGTGTGACTTACCTCT</dnaseq><br />
<br />
<br />
==Labs working on this lncRNA==<br />
* Division for Therapies against Intractable Diseases, Institute for Comprehensive Medical Science (ICMS), Fujita Health University, Toyoake, Japan.<br />
* Department of Medical Technology, School of Health Sciences, Gifu University of Medical Science, Seki, Japan.<br />
<br />
==References==<br />
<references><br />
<ref name="ref1"><br />
Keisuke Hitachi, Masashi Nakatani, Akihiko Takasaki,Yuya Ouchi, Akiyoshi,Uezumi1, Hiroshi Ageta1, Hidehito Inagaki,Hiroki Kurahashi & Kunihiro Tsuchida1. Myogenin promoter‐associated lncRNA Myoparr is essential for myogenic differentiation.EMBO reports,2019 Mar;20(3).<br />
</ref>(1)<br />
</references></div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=Lnc-LRR1-1:1&diff=1276404Lnc-LRR1-1:12019-08-12T04:06:27Z<p>Qianpeng Li: /* Name */</p>
<hr />
<div>==Annotated Information==<br />
===Name===<br />
Approved symbol: RN7SL1<br />
<br />
Approved name: RNA component of signal recognition particle 7SL1<br />
<br />
Previous symbols: RN7SL<br />
<br />
Alias symbols: 7SL, 7L1a, RNSRP1<br />
<br />
LncBook transcript ID: HSALNT0289533<br />
<br />
===Characteristics===<br />
~300 nt, transcribed by RNAPIII. <br />
<br />
The eukaryotic small cytoplasmic 7SL is an RNA component of the SRP (signal recognition particle), which associates with the ribosome and targets nascent proteins to the endoplasmic reticulum for secretion or membrane insertion ([http://www.ncbi.nlm.nih.gov/pubmed/6181418 (Walter 1982)]) ([http://www.ncbi.nlm.nih.gov/pubmed/15611297 (Zwieb 2004)]).<br />
<br />
===Expression===<br />
Ubiquitously expressed at high levels. Localises to the cytoplasm. An expression profile from 11 human tissues using RNA sequencing showed 7SL was most highly expressed ncRNA and could be an order of magnitude more highly expressed than any mRNA ([http://www.ncbi.nlm.nih.gov/pubmed/20668672 (Castle 2010)]).<br />
<br />
===Regulation===<br />
* Activating transcription factor (ATF), in the 5′ flanking region of 7S L RNA gene between –43 and –50 upstream of the transcription start site, is involved in the regulation of human 7S L RNA transcription by RNA polymerase III in vivo and in vitro([https://www.ncbi.nlm.nih.gov/pubmed/1702200 (Bredow 2004)]).<br />
<br />
[[File:Re seq of RNA7SL.png|right|thumb|Schematic presentation of promoter elements utilized by pol III for basal transcription of the human 7SL RNA genes Hs7SL-1 and Hs7SL-3 in HeLa<br />
nuclear extract([https://www.ncbi.nlm.nih.gov/pubmed/15667936 (Englert 2004)])]]<br />
<br />
* It is reported that a TATA-like sequence located approximately between –20 and –30 upstream of the coding regions of Hs7SL-1 as well as internal A and B box-like motifs are important in the transcription of human 7SL RNA genes([https://www.ncbi.nlm.nih.gov/pubmed/15667936 (Englert 2004)]).<br />
<br />
===Function===<br />
* 7SL RNA is required for structural and functional properties of SRP ([http://www.ncbi.nlm.nih.gov/pubmed/6181418 (Walter 1982)]), being a scaffold component upon which the six proteins of the SRP bind in higher eukaryotes. In mammals SRP consists of the SRP RNA the six proteins named SRP9, SRP14, SRP19, SRP54, SRP68, and SRP72 ([http://www.ncbi.nlm.nih.gov/pubmed/6196367 (Walter 1983)]).<br />
<br />
* Bacterial SRP has a much reduced complexity, consisting of a small SRP RNA (4.5S RNA) and a homolog of protein SRP54, also called Ffh or P48 ([http://www.ncbi.nlm.nih.gov/pubmed/8389475 (Bernstein 1993)]). In archaea only two SRP proteins, SRP19 and SRP54, are thought to be part of the SRP, although SRP RNA closely resembles the mammalian homolog ([http://www.ncbi.nlm.nih.gov/pubmed/10684931 (Bhuiyan 2000)]).<br />
<br />
* There is evidence that a highly conserved region of 7SL RNA catalyses the binding of SRP to its receptor SR, and that this RNA stimulates the GTPase activities of the SRP-SR complex ([http://www.ncbi.nlm.nih.gov/pubmed/18617187 (Zhang 2008)]) ([http://www.ncbi.nlm.nih.gov/pubmed/17164479 (Siu 2006)]) ([http://www.ncbi.nlm.nih.gov/pubmed/10834842 (Peluso 2000)]).<br />
<br />
===Disease===<br />
AIDS <ref name="ref1" /> <ref name="ref2" /><br />
<br />
===Evolution===<br />
Please input evolution information here.<br />
<br />
==Labs working on this lncRNA==<br />
* Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan, USA.<ref name="ref1" /><br />
* Laboratory of Cellular Biophysics, The Rockefeller University, New York, New York.<ref name="ref2" /><br />
<br />
==References==<br />
<references><br />
<ref name="ref1"> Keene SE, King SR, Telesnitsky A. 7SL RNA is retained in HIV-1 minimal<br />
virus-like particles as an S-domain fragment. J Virol. 2010 Sep;84(18):9070-7.<br />
doi: 10.1128/JVI.00714-10.<br />
</ref>(1)<br />
<ref name="ref2"> Itano MS, Arnion H, Wolin SL, Simon SM. Recruitment of 7SL RNA to assembling<br />
HIV-1 virus-like particles. Traffic. 2018 Jan;19(1):36-43. doi:<br />
10.1111/tra.12536.<br />
</ref>(2)<br />
</references><br />
[http://www.lncrnadb.org/7SL/ Annotation originally sourced from lncRNAdb.]<br />
<br />
{{basic|<br />
tID = lnc-LRR1-1:1|<br />
source = LNCipedia2.1|<br />
same = ,|<br />
classification = intergenic|<br />
length = 299 nt|<br />
location = chr14+:50053297..50053596|<br />
number = 1|<br />
exons = 50053297..50053596|<br />
context = <html><div align="center"><br />
<iframe src="http://lncrna.big.ac.cn/view/?data=species/human&loc=chr14:50053297..50053596&tracklist=0&overview=0&tracks=DNA,RefGene,lncRNA" style=" border-width:0 " width="100%" height="250" scrolling="yes"></iframe><br />
</div></html>|<br />
sequence = <dnaseq>GCCGGGCGCGGTGGCGCGTGCCTGTAGTCCCAGCTACTCGGGAGGCTGAGGCTGGAGGATCGCTTGAGTCCAGGAGTTCTGGGCTGTAGTGCGCTATGCCGATCGGGTGTCCGCACTAAGTTCGGCATCAATATGGTGACCTCCCGGGAGCGGGGGACCACCAGGTTGCCTAAGGAGGGGTGAACCGGCCCAGGTCGGAAACGGAGCAGGTCAAAACTCCCGTGCTGATCAGTAGTGGGATCGCGCCTGTGAATAGCCACTGCACTCCAGCCTGGGCAACATAGCGAGACCCCGTCTCT</dnaseq>|<br />
}}<br />
[[Category:Intergenic]][[Category:lnc-LRR1-1]][[Category:Transcripts]]</div>Qianpeng Lihttps://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=DEC1&diff=1276403DEC12019-08-12T04:03:10Z<p>Qianpeng Li: </p>
<hr />
<div>''DEC1'', a candidate tumor suppressor in 9q32<br />
==Annotated Information==<br />
===Name===<br />
Approved symbol: DEC1<br />
<br />
Approved name: deleted in esophageal cancer 1<br />
<br />
HGNC ID: HGNC: 23658<br />
<br />
Aliases: CTS9, Candidate Tumor Suppressor CTS9<br />
<br />
RefSeq ID: NR_163556<br />
<br />
<br />
<br />
===Characteristics===<br />
<br />
<br />
===Function===<br />
''DEC1'' cDNA can suppress growth of some cancer cells in vitro, it is a candidate tumor suppressor in 9q32 <ref name="ref1" />.<br />
<br />
<br />
===Regulation===<br />
<br />
<br />
===Disease=== <br />
*esophageal squamous cell carcinoma <ref name="ref1" /><ref name="ref2" /><br />
<br />
===Expression===<br />
The DEC1 gene is expressed in most normal human tissues, including the esophagus, but its expression is lower than normal, often absent, in more than half of the esophageal carcinomas examined <ref name="ref1" />.<br />
===Sequence===<br />
>PREDICTED: Homo sapiens deleted in esophageal cancer 1 (DEC1), transcript variant X1<br />
<dnaseq> CTTCCAGTTCTGGAGGCTGGGAAGTGGAAGAGCATTGTGCCAGCACCTGGTGAGGGCCTTCTTGCCGTGT<br />
TACACATGATGGTTTTTACTGATGCCCTGCACAGAGAGAGGTCTGTAAAGTGGCAAGCAGGAGTCTGCTA<br />
CAATGGAGGAAAGGATTTTGCTGTATCTCTTGCCAGGCCCAAGGCTGCAGAGGGAATTGGTAATATACTT<br />
CATTTAATAATAGTGTTTTAAGGGACATTATCATTTCATCCTATGTGGTAGATGTGATCATCTTCATCTC<br />
ACAGATGAAAAGAGACAAACCTGGGATTCAGAGGTACTTGCCTATGAGTTTCTTACAGATTTCCTCTTAC<br />
AATCCAGAACTGCTGATTCCTGGGTCAGTGTCCTTTCCAATATGGCATCTTAGGCATGGCAATAAGTGAG<br />
ATCTAAAAGCTAGTTATTTGATGCTTGGACAAAGGCTTAGGGCATGGGCTTTGACCTAATGAATCAGTAG<br />
ATTCTAGTCTAATATTTTAAAGGATTTGAAATGATTCCAGTTTATAAGCCCCTTTAACTGTCTTCTAAGA<br />
TGTGGCTAAACATTCCAACCTTCCTTAGCTCAAAAGTGGACAAAACAAGAGATTACACATGTTGATACTT<br />
TGGGAGTCATAGAAAATTCACATATACATAGGCAGAGTGGTTCTGTAATTAACCAAATCTTTAGAGGTCC<br />
AAGGTTAACAGTATTGACCATTCATAATTAGCCATAAACTCAGACATTTTAAAAGCCTCATGAAAATAGA<br />
AGTATAGTTTTCAAATGTTACAGACCCCAAACACCAGTGTTTTATTGCCTACAGCAAGCATAGCTCACAG<br />
ATCATCAC</dnaseq><br />
==Labs working on this lncRNA==<br />
*Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, University of Tokyo, Tokyo, Japan.<br />
*Laboratory of Molecular Medicine, The Institute of Medical Science, The University of Tokyo, Japan.<br />
<br />
<br />
==References==<br />
<references><br />
<ref name="ref1"> Nishiwaki T, Daigo Y, Kawasoe T, Nakamura Y. Isolation and mutational analysis of a novel human cDNA, DEC1 (deleted in esophageal cancer 1), derived from the tumor suppressor locus in 9q32. Genes Chromosomes Cancer. 2000 Feb;27(2):169-76.</ref>(1)<br />
<ref name="ref2">Miura K, Suzuki K, Tokino T, Isomura M, Inazawa J, Matsuno S, Nakamura Y. Detailed deletion mapping in squamous cell carcinomas of the esophagus narrows a region containing a putative tumor suppressor gene to about 200 kilobases on distal chromosome 9q. Cancer Res. 1996 Apr 1;56(7):1629-34.</ref>(2)<br />
</references></div>Qianpeng Li