Difference between revisions of "ENST00000534336.1"

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<ref name="ref1">Ji, P., Diederichs, S., Wang, W., Boing, S., Metzger, R., Schneider, P.M., Tidow, N., Brandt, B., Buerger, H., Bulk, E. et al. (2003) MALAT-1, a novel noncoding RNA, and thymosin beta4 predict metastasis and survival in early-stage non-small cell lung cancer. Oncogene, 22, 8031-8041.</ref>
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Revision as of 09:27, 27 June 2014

Please input one-sentence summary here.

Annotated Information

Transcriptomic Nomeclature

hsa-N11QT0652001-SSCY-LMXXX01

Name

Malat1: Metastasis-associated lung adenocarcinoma transcript 1

Neat2: Nuclear enriched abundant transcript 2

Characteristics

Malat1 gene is localized in the intergenic region of the genome. It is about 8kb in length and the transcript has only one exon (1,2). The 3’-end of the transcript is a conserved tRNA-like sequence, which can be modified by RNase P and cleaved by RNase Z to yield another ncRNA, the cytoplasmic MALAT1-associated small cytoplasmic RNA (mascRNA) (3).

Malat1 is stable in human B cells (half-life: 16.5 h) (4) and Hela cells (half-life: about 7 h) (5), but is unstable in mouse 3T3 cells (half-life: 3 h) (4) and N2A cells ( half-life: 4 h) (4). MALAT-1 is generally stable in cancer cells, with the half-life ranging from ~ 9 h to > 12 h in various cancer cells (6). Xrn2, PM/Scl-75, PARN, and Mtr4, known nuclear RNases or RNA helicases, do not affect MALAT-1 degradation (6).

Cellular localization

MALAT-1 localize predominately in the nucleus . In G2/M cell cycle phase, MALAT-1 transcripts partially translocate from the nucleus into the cytoplasm (4). RNPS1, SRm160, and IBP160 are found to contribute to the nuclear localization of MALAT-1 (5).

Function

Figure 1. Hypothetical model depicting the role of MALAT1 in AS (alternative splicing) regulation. (Ea) In normal cells, MALAT1, by associating with SR proteins in nuclear speckles and in the nucleoplasm, regulates their recruitment to the pre-mRNA, thereby regulating AS. Here we have shown SAT1 pre-mRNA as an example that undergoes alternate exon exclusion in normal cells. However, in MALAT1-depleted cells (Eb), cellular levels of SR proteins are increased and are also present predominantly in the dephosphorylated form, resulting in changes in AS of pre-mRNA. In case of SAT1 pre-mRNA, MALAT1 depletion results in the inclusion of an alternative exon containing weak splice sites. (from reference [1]).

MALAT-1 could modulate mRNA alternative splicing via its interaction with the serine/arginine-rich (SR) family of nuclear phosphoproteins that are involved in the splicing machinery (6). It is found that Malat1 regulates synapse formation by modulating the expression of genes involved in synapse formation and/or maintenance (10). However, splicing alterations were not found after Malat1 ablation in mice (7). Also, MALAT1 does not alter alternative splicing but actively regulates gene expression including a set of metastasis-associated genes in lung cancer cells (8). These results indicate that alternative functions for MALAT-1 may exist.

MALAT-1 can function by participating in localization of important proteins, such as hnRNP C (7) and growth control genes (13). MALAT-1 is found to regulate cell cycle progress in G2/M phase (4,6), G1/S phase (9), and G0/G1 phase (10). In the G2/M phase, MALAT-1 interacts with hnRNP C to facilitate the cytoplasmic translocation of hnRNP C, leading to cell cycle progresion (7). MALAT1 could interact with the demethylated form of CBX4 (chromobox homolog 4), and controls the relocalization of growth control genes between polycomb bodies and interchromatin granules (13). MALAT1 could bind to Human PSF protein to release hPSF from a repressed proto-oncogene and activate transcription, driving transformation and tumorigenesis (16).

MALAT-1 regulates synaptogenesis (10)and is involved in the development of advanced invasive placentation (17). Deregulation of MALAT-1 is found to be closely associated with the development of cancer. In vitro, it is found that MALAT-1 promotes epithelial–mesenchymal transition (EMT) of bladder cancer cells by activating Wnt signaling (12). 3' end of MALAT-1 (6918 nt-8441 nt) is found to be important in colorectal cancer metastasis (19). In lung adenocarcinoma cells, MALAT-1 may regulate cell motility through transcriptional and post-transcriptional regulation of motility related gene expression (20). However, mechanisms of these regulations are not clear.

Regulation

In breast cancer cells, high concentration E2 treatment largely decreases MALAT-1 RNA level in an ERa independent way (25).

Disruption of p53 appears to play an important role in the up-regulation of MALAT-1 (26).

CREB is found to bind to the defined proximal promoter of the MALAT1 gene, leading to the up-regulation of MALAT1 (27).

Diseases

MALAT-1 was first identified as a prognostic marker for metastasis and patient survival in non-small cell lung cancer (NSCLC) (28). It is found to be overexpressed in various tumors and cancer cell lines, including NSCLC (1,28), endometrial stromal sarcoma of the uterus (29), hepatocellular carcinomas (30,31), breast cancer (32), prostate cancer (15), melanoma (22), bladder cancer (18). Overexpression of MALAT-1 in cancer cells is closely associated with tumor growth and metastasis (12,20,22,28).

There is no significant difference in MALAT-1 lncRNA levels in normal pituitary tissues, invasive NFPAs (non-functioning pituitary adenomas), and non-invasive NFPAs, and no significant association between MALAT-1 expression and patient clinicopathological characteristics (23).

Expression

MALAT-1 is highly and ubiquity expressed in various tissue (10), including both cancer tissues and normal tissues, such as brain (10). It is found to be up-regulated in the cerebellum, hippocampus and brain stem of human alcoholics (21).

Primer Forward primer Reverse primer
RT-PCR 5'-AAAGCAAGGTCTCCCCACAAG-3' 5'-GGTCTGTGCTAGATCAAAAGGCA-3' ( [2][3])
5'-CTTCCCTAGGGGATTTCAGG-3' 5'-GCCCACAGGAACAAGTCCTA-3' ( [4])
5'-GAATTGCGTCATTTAAAGCCTAGTT-3' 5'-GTTTCATCCTACCACTCCCAATTAAT-3' ( [5])
5'-cggaagtaattcaagatcaagag-3' 5'-actgaatccacttctgtgtagc-3' ( [6])
cDNA amplication 5'-GTAGGGCCCTCCATGGCGATTTGCCTTGTGAGCAC-3' 5'-GAGCTCGAGGTCCTGAAGACAGATTAGTAGTCAAAGC-3' [7]

Allelic Information and Variation

Please input allelic information and variation information here.

Evolution

MALAT-1 is highly conserved over its full length (~8 kb) across mammals (10). However, sequence conservation is limited in vertebrates. Sequence similarity between zebrafish and mammalian MALAT1 is restricted to the 3′ end, while the length of MALAT1 (~7 kb) along with the gene structure appeare to be roughly fixed in all vertebrates (14).

Associated components

MALAT-1 is an 8-knt-long macromolecule that can form a complex structure to recruit many different protein factors for functionality. MALAT-1 is found to interact with hnRNP C and facilitate its cytoplasmic translocation in the G2/M phase, thereby regulating the progress of the cell cycle (4).

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Labs working on this lncRNA

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References

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  2. Cite error: Invalid <ref> tag; no text was provided for refs named ref_22
  3. Cite error: Invalid <ref> tag; no text was provided for refs named ref_23
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  6. Cite error: Invalid <ref> tag; no text was provided for refs named ref_16
  7. Cite error: Invalid <ref> tag; no text was provided for refs named ref_6

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Basic Information

Transcript ID

ENST00000534336.1

Source

{{{source}}}

Same with

lnc-SCYL1-1:2;n343070;Malat1(NR_002819.2)

Classification

intergenic

Length

{{{length}}}

Genomic location

chr11+:65265233-65273940

Exon number

{{{number}}}

Exons

{{{exons}}}

Genome context

{{{context}}}

Sequence
000001 GTAAAGGACT GGGGCCCCGC AACTGGCCTC TCCTGCCCTC TTAAGCGCAG CGCCATTTTA GCAACGCAGA AGCCCGGCGC 000080
000081 CGGGAAGCCT CAGCTCGCCT GAAGGCAGGT CCCCTCTGAC GCCTCCGGGA GCCCAGGTTT CCCAGAGTCC TTGGGACGCA 000160
000161 GCGACGAGTT GTGCTGCTAT CTTAGCTGTC CTTATAGGCT GGCCATTCCA GGTGGTGGTA TTTAGATAAA ACCACTCAAA 000240
000241 CTCTGCAGTT TGGTCTTGGG GTTTGGAGGA AAGCTTTTAT TTTTCTTCCT GCTCCGGTTC AGAAGGTCTG AAGCTCATAC 000320
000321 CTAACCAGGC ATAACACAGA ATCTGCAAAA CAAAAACCCC TAAAAAAGCA GACCCAGAGC AGTGTAAACA CTTCTGGGTG 000400
000401 TGTCCCTGAC TGGCTGCCCA AGGTCTCTGT GTCTTCGGAG ACAAAGCCAT TCGCTTAGTT GGTCTACTTT AAAAGGCCAC 000480
000481 TTGAACTCGC TTTCCATGGC GATTTGCCTT GTGAGCACTT TCAGGAGAGC CTGGAAGCTG AAAAACGGTA GAAAAATTTC 000560
000561 CGTGCGGGCC GTGGGGGGCT GGCGGCAACT GGGGGGCCGC AGATCAGAGT GGGCCACTGG CAGCCAACGG CCCCCGGGGC 000640
000641 TCAGGCGGGG AGCAGCTCTG TGGTGTGGGA TTGAGGCGTT TTCCAAGAGT GGGTTTTCAC GTTTCTAAGA TTTCCCAAGC 000720
000721 AGACAGCCCG TGCTGCTCCG ATTTCTCGAA CAAAAAAGCA AAACGTGTGG CTGTCTTGGG AGCAAGTCGC AGGACTGCAA 000800
000801 GCAGTTGGGG GAGAAAGTCC GCCATTTTGC CACTTCTCAA CCGTCCCTGC AAGGCTGGGG CTCAGTTGCG TAATGGAAAG 000880
000881 TAAAGCCCTG AACTATCACA CTTTAATCTT CCTTCAAAAG GTGGTAAACT ATACCTACTG TCCCTCAAGA GAACACAAGA 000960
000961 AGTGCTTTAA GAGGTATTTT AAAAGTTCCG GGGGTTTTGT GAGGTGTTTG ATGACCCGTT TAAAATATGA TTTCCATGTT 001040
001041 TCTTTTGTCT AAAGTTTGCA GCTCAAATCT TTCCACACGC TAGTAATTTA AGTATTTCTG CATGTGTAGT TTGCATTCAA 001120
001121 GTTCCATAAG CTGTTAAGAA AAATCTAGAA AAGTAAAACT AGAACCTATT TTTAACCGAA GAACTACTTT TTGCCTCCCT 001200
001201 CACAAAGGCG GCGGAAGGTG ATCGAATTCC GGTGATGCGA GTTGTTCTCC GTCTATAAAT ACGCCTCGCC CGAGCTGTGC 001280
001281 GGTAGGCATT GAGGCAGCCA GCGCAGGGGC TTCTGCTGAG GGGGCAGGCG GAGCTTGAGG AAACCGCAGA TAAGTTTTTT 001360
001361 TCTCTTTGAA AGATAGAGAT TAATACAACT ACTTAAAAAA TATAGTCAAT AGGTTACTAA GATATTGCTT AGCGTTAAGT 001440
001441 TTTTAACGTA ATTTTAATAG CTTAAGATTT TAAGAGAAAA TATGAAGACT TAGAAGAGTA GCATGAGGAA GGAAAAGATA 001520
001521 AAAGGTTTCT AAAACATGAC GGAGGTTGAG ATGAAGCTTC TTCATGGAGT AAAAAATGTA TTTAAAAGAA AATTGAGAGA 001600
001601 AAGGACTACA GAGCCCCGAA TTAATACCAA TAGAAGGGCA ATGCTTTTAG ATTAAAATGA AGGTGACTTA AACAGCTTAA 001680
001681 AGTTTAGTTT AAAAGTTGTA GGTGATTAAA ATAATTTGAA GGCGATCTTT TAAAAAGAGA TTAAACCGAA GGTGATTAAA 001760
001761 AGACCTTGAA ATCCATGACG CAGGGAGAAT TGCGTCATTT AAAGCCTAGT TAACGCATTT ACTAAACGCA GACGAAAATG 001840
001841 GAAAGATTAA TTGGGAGTGG TAGGATGAAA CAATTTGGAG AAGATAGAAG TTTGAAGTGG AAAACTGGAA GACAGAAGTA 001920
001921 CGGGAAGGCG AAGAAAAGAA TAGAGAAGAT AGGGAAATTA GAAGATAAAA ACATACTTTT AGAAGAAAAA AGATAAATTT 002000
002001 AAACCTGAAA AGTAGGAAGC AGAAGAAAAA AGACAAGCTA GGAAACAAAA AGCTAAGGGC AAAATGTACA AACTTAGAAG 002080
002081 AAAATTGGAA GATAGAAACA AGATAGAAAA TGAAAATATT GTCAAGAGTT TCAGATAGAA AATGAAAAAC AAGCTAAGAC 002160
002161 AAGTATTGGA GAAGTATAGA AGATAGAAAA ATATAAAGCC AAAAATTGGA TAAAATAGCA CTGAAAAAAT GAGGAAATTA 002240
002241 TTGGTAACCA ATTTATTTTA AAAGCCCATC AATTTAATTT CTGGTGGTGC AGAAGTTAGA AGGTAAAGCT TGAGAAGATG 002320
002321 AGGGTGTTTA CGTAGACCAG AACCAATTTA GAAGAATACT TGAAGCTAGA AGGGGAAGTT GGTTAAAAAT CACATCAAAA 002400
002401 AGCTACTAAA AGGACTGGTG TAATTTAAAA AAAACTAAGG CAGAAGGCTT TTGGAAGAGT TAGAAGAATT TGGAAGGCCT 002480
002481 TAAATATAGT AGCTTAGTTT GAAAAATGTG AAGGACTTTC GTAACGGAAG TAATTCAAGA TCAAGAGTAA TTACCAACTT 002560
002561 AATGTTTTTG CATTGGACTT TGAGTTAAGA TTATTTTTTA AATCCTGAGG ACTAGCATTA ATTGACAGCT GACCCAGGTG 002640
002641 CTACACAGAA GTGGATTCAG TGAATCTAGG AAGACAGCAG CAGACAGGAT TCCAGGAACC AGTGTTTGAT GAAGCTAGGA 002720
002721 CTGAGGAGCA AGCGAGCAAG CAGCAGTTCG TGGTGAAGAT AGGAAAAGAG TCCAGGAGCC AGTGCGATTT GGTGAAGGAA 002800
002801 GCTAGGAAGA AGGAAGGAGC GCTAACGATT TGGTGGTGAA GCTAGGAAAA AGGATTCCAG GAAGGAGCGA GTGCAATTTG 002880
002881 GTGATGAAGG TAGCAGGCGG CTTGGCTTGG CAACCACACG GAGGAGGCGA GCAGGCGTTG TGCGTAGAGG ATCCTAGACC 002960
002961 AGCATGCCAG TGTGCCAAGG CCACAGGGAA AGCGAGTGGT TGGTAAAAAT CCGTGAGGTC GGCAATATGT TGTTTTTCTG 003040
003041 GAACTTACTT ATGGTAACCT TTTATTTATT TTCTAATATA ATGGGGGAGT TTCGTACTGA GGTGTAAAGG GATTTATATG 003120
003121 GGGACGTAGG CCGATTTCCG GGTGTTGTAG GTTTCTCTTT TTCAGGCTTA TACTCATGAA TCTTGTCTGA AGCTTTTGAG 003200
003201 GGCAGACTGC CAAGTCCTGG AGAAATAGTA GATGGCAAGT TTGTGGGTTT TTTTTTTTTA CACGAATTTG AGGAAAACCA 003280
003281 AATGAATTTG ATAGCCAAAT TGAGACAATT TCAGCAAATC TGTAAGCAGT TTGTATGTTT AGTTGGGGTA ATGAAGTATT 003360
003361 TCAGTTTTGT GAATAGATGA CCTGTTTTTA CTTCCTCACC CTGAATTCGT TTTGTAAATG TAGAGTTTGG ATGTGTAACT 003440
003441 GAGGCGGGGG GGAGTTTTCA GTATTTTTTT TTGTGGGGGT GGGGGCAAAA TATGTTTTCA GTTCTTTTTC CCTTAGGTCT 003520
003521 GTCTAGAATC CTAAAGGCAA ATGACTCAAG GTGTAACAGA AAACAAGAAA ATCCAATATC AGGATAATCA GACCACCACA 003600
003601 GGTTTACAGT TTATAGAAAC TAGAGCAGTT CTCACGTTGA GGTCTGTGGA AGAGATGTCC ATTGGAGAAA TGGCTGGTAG 003680
003681 TTACTCTTTT TTCCCCCCAC CCCCTTAATC AGACTTTAAA AGTGCTTAAC CCCTTAAACT TGTTATTTTT TACTTGAAGC 003760
003761 ATTTTGGGAT GGTCTTAACA GGGAAGAGAG AGGGTGGGGG AGAAAATGTT TTTTTCTAAG ATTTTCCACA GATGCTATAG 003840
003841 TACTATTGAC AAACTGGGTT AGAGAAGGAG TGTACCGCTG TGCTGTTGGC ACGAACACCT TCAGGGACTG GAGCTGCTTT 003920
003921 TATCCTTGGA AGAGTATTCC CAGTTGAAGC TGAAAAGTAC AGCACAGTGC AGCTTTGGTT CATATTCAGT CATCTCAGGA 004000
004001 GAACTTCAGA AGAGCTTGAG TAGGCCAAAT GTTGAAGTTA AGTTTTCCAA TAATGTGACT TCTTAAAAGT TTTATTAAAG 004080
004081 GGGAGGGGCA AATATTGGCA ATTAGTTGGC AGTGGCCTGT TACGGTTGGG ATTGGTGGGG TGGGTTTAGG TAATTGTTTA 004160
004161 GTTTATGATT GCAGATAAAC TCATGCCAGA GAACTTAAAG TCTTAGAATG GAAAAAGTAA AGAAATATCA ACTTCCAAGT 004240
004241 TGGCAAGTAA CTCCCAATGA TTTAGTTTTT TTCCCCCCAG TTTGAATTGG GAAGCTGGGG GAAGTTAAAT ATGAGCCACT 004320
004321 GGGTGTACCA GTGCATTAAT TTGGGCAAGG AAAGTGTCAT AATTTGATAC TGTATCTGTT TTCCTTCAAA GTATAGAGCT 004400
004401 TTTGGGGAAG GAAAGTATTG AACTGGGGGT TGGTCTGGCC TACTGGGCTG ACATTAACTA CAATTATGGG AAATGCAAAA 004480
004481 GTTGTTTGGA TATGGTAGTG TGTGGTTCTC TTTTGGAATT TTTTTCAGGT GATTTAATAA TAATTTAAAA CTACTATAGA 004560
004561 AACTGCAGAG CAAAGGAAGT GGCTTAATGA TCCTGAAGGG ATTTCTTCTG ATGGTAGCTT TTGTATTATC AAGTAAGATT 004640
004641 CTATTTTCAG TTGTGTGTAA GCAAGTTTTT TTTTAGTGTA GGAGAAATAC TTTTCCATTG TTTAACTGCA AAACAAGATG 004720
004721 TTAAGGTATG CTTCAAAAAT TTTGTAAATT GTTTATTTTA AACTTATCTG TTTGTAAATT GTAACTGATT AAGAATTGTG 004800
004801 ATAGTTCAGC TTGAATGTCT CTTAGAGGGT GGGCTTTTGT TGATGAGGGA GGGGAAACTT TTTTTTTTTC TATAGACTTT 004880
004881 TTTCAGATAA CATCTTCTGA GTCATAACCA GCCTGGCAGT ATGATGGCCT AGATGCAGAG AAAACAGCTC CTTGGTGAAT 004960
004961 TGATAAGTAA AGGCAGAAAA GATTATATGT CATACCTCCA TTGGGGAATA AGCATAACCC TGAGATTCTT ACTACTGATG 005040
005041 AGAACATTAT CTGCATATGC CAAAAAATTT TAAGCAAATG AAAGCTACCA ATTTAAAGTT ACGGAATCTA CCATTTTAAA 005120
005121 GTTAATTGCT TGTCAAGCTA TAACCACAAA AATAATGAAT TGATGAGAAA TACAATGAAG AGGCAATGTC CATCTCAAAA 005200
005201 TACTGCTTTT ACAAAAGCAG AATAAAAGCG AAAAGAAATG AAAATGTTAC ACTACATTAA TCCTGGAATA AAAGAAGCCG 005280
005281 AAATAAATGA GAGATGAGTT GGGATCAAGT GGATTGAGGA GGCTGTGCTG TGTGCCAATG TTTCGTTTGC CTCAGACAGG 005360
005361 TATCTCTTCG TTATCAGAAG AGTTGCTTCA TTTCATCTGG GAGCAGAAAA CAGCAGGCAG CTGTTAACAG ATAAGTTTAA 005440
005441 CTTGCATCTG CAGTATTGCA TGTTAGGGAT AAGTGCTTAT TTTTAAGAGC TGTGGAGTTC TTAAATATCA ACCATGGCAC 005520
005521 TTTCTCCTGA CCCCTTCCCT AGGGGATTTC AGGATTGAGA AATTTTTCCA TCGAGCCTTT TTAAAATTGT AGGACTTGTT 005600
005601 CCTGTGGGCT TCAGTGATGG GATAGTACAC TTCACTCAGA GGCATTTGCA TCTTTAAATA ATTTCTTAAA AGCCTCTAAA 005680
005681 GTGATCAGTG CCTTGATGCC AACTAAGGAA ATTTGTTTAG CATTGAATCT CTGAAGGCTC TATGAAAGGA ATAGCATGAT 005760
005761 GTGCTGTTAG AATCAGATGT TACTGCTAAA ATTTACATGT TGTGATGTAA ATTGTGTAGA AAACCATTAA ATCATTCAAA 005840
005841 ATAATAAACT ATTTTTATTA GAGAATGTAT ACTTTTAGAA AGCTGTCTCC TTATTTAAAT AAAATAGTGT TTGTCTGTAG 005920
005921 TTCAGTGTTG GGGCAATCTT GGGGGGGATT CTTCTCTAAT CTTTCAGAAA CTTTGTCTGC GAACACTCTT TAATGGACCA 006000
006001 GATCAGGATT TGAGCGGAAG AACGAATGTA ACTTTAAGGC AGGAAAGACA AATTTTATTC TTCATAAAGT GATGAGCATA 006080
006081 TAATAATTCC AGGCACATGG CAATAGAGGC CCTCTAAATA AGGAATAAAT AACCTCTTAG ACAGGTGGGA GATTATGATC 006160
006161 AGAGTAAAAG GTAATTACAC ATTTTATTTC CAGAAAGTCA GGGGTCTATA AATTGACAGT GATTAGAGTA ATACTTTTTC 006240
006241 ACATTTCCAA AGTTTGCATG TTAACTTTAA ATGCTTACAA TCTTAGAGTG GTAGGCAATG TTTTACACTA TTGACCTTAT 006320
006321 ATAGGGAAGG GAGGGGGTGC CTGTGGGGTT TTAAAGAATT TTCCTTTGCA GAGGCATTTC ATCCTTCATG AAGCCATTCA 006400
006401 GGATTTTGAA TTGCATATGA GTGCTTGGCT CTTCCTTCTG TTCTAGTGAG TGTATGAGAC CTTGCAGTGA GTTTATCAGC 006480
006481 ATACTCAAAA TTTTTTTCCT GGAATTTGGA GGGATGGGAG GAGGGGGTGG GGCTTACTTG TTGTAGCTTT TTTTTTTTTT 006560
006561 ACAGACTTCA CAGAGAATGC AGTTGTCTTG ACTTCAGGTC TGTCTGTTCT GTTGGCAAGT AAATGCAGTA CTGTTCTGAT 006640
006641 CCCGCTGCTA TTAGAATGCA TTGTGAAACG ACTGGAGTAT GATTAAAAGT TGTGTTCCCC AATGCTTGGA GTAGTGATTG 006720
006721 TTGAAGGAAA AAATCCAGCT GAGTGATAAA GGCTGAGTGT TGAGGAAATT TCTGCAGTTT TAAGCAGTCG TATTTGTGAT 006800
006801 TGAAGCTGAG TACATTTTGC TGGTGTATTT TTAGGTAAAA TGCTTTTTGT TCATTTCTGG TGGTGGGAGG GGACTGAAGC 006880
006881 CTTTAGTCTT TTCCAGATGC AACCTTAAAA TCAGTGACAA GAAACATTCC AAACAAGCAA CAGTCTTCAA GAAATTAAAC 006960
006961 TGGCAAGTGG AAATGTTTAA ACAGTTCAGT GATCTTTAGT GCATTGTTTA TGTGTGGGTT TCTCTCTCCC CTCCCTTGGT 007040
007041 CTTAATTCTT ACATGCAGGA ACACTCAGCA GACACACGTA TGCGAAGGGC CAGAGAAGCC AGACCCAGTA AGAAAAAATA 007120
007121 GCCTATTTAC TTTAAATAAA CCAAACATTC CATTTTAAAT GTGGGGATTG GGAACCACTA GTTCTTTCAG ATGGTATTCT 007200
007201 TCAGACTATA GAAGGAGCTT CCAGTTGAAT TCACCAGTGG ACAAAATGAG GAAAACAGGT GAACAAGCTT TTTCTGTATT 007280
007281 TACATACAAA GTCAGATCAG TTATGGGACA ATAGTATTGA ATAGATTTCA GCTTTATGCT GGAGTAACTG GCATGTGAGC 007360
007361 AAACTGTGTT GGCGTGGGGG TGGAGGGGTG AGGTGGGCGC TAAGCCTTTT TTTAAGATTT TTCAGGTACC CCTCACTAAA 007440
007441 GGCACCGAAG GCTTAAAGTA GGACAACCAT GGAGCCTTCC TGTGGCAGGA GAGACAACAA AGCGCTATTA TCCTAAGGTC 007520
007521 AAGAGAAGTG TCAGCCTCAC CTGATTTTTA TTAGTAATGA GGACTTGCCT CAACTCCCTC TTTCTGGAGT GAAGCATCCG 007600
007601 AAGGAATGCT TGAAGTACCC CTGGGCTTCT CTTAACATTT AAGCAAGCTG TTTTTATAGC AGCTCTTAAT AATAAAGCCC 007680
007681 AAATCTCAAG CGGTGCTTGA AGGGGAGGGA AAGGGGGAAA GCGGGCAACC ACTTTTCCCT AGCTTTTCCA GAAGCCTGTT 007760
007761 AAAAGCAAGG TCTCCCCACA AGCAACTTCT CTGCCACATC GCCACCCCGT GCCTTTTGAT CTAGCACAGA CCCTTCACCC 007840
007841 CTCACCTCGA TGCAGCCAGT AGCTTGGATC CTTGTGGGCA TGATCCATAA TCGGTTTCAA GGTAACGATG GTGTCGAGGT 007920
007921 CTTTGGTGGG TTGAACTATG TTAGAAAAGG CCATTAATTT GCCTGCAAAT TGTTAACAGA AGGGTATTAA AACCACAGCT 008000
008001 AAGTAGCTCT ATTATAATAC TTATCCAGTG ACTAAAACCA ACTTAAACCA GTAAGTGGAG AAATAACATG TTCAAGAACT 008080
008081 GTAATGCTGG GTGGGAACAT GTAACTTGTA GACTGGAGAA GATAGGCATT TGAGTGGCTG AGAGGGCTTT TGGGTGGGAA 008160
008161 TGCAAAAATT CTCTGCTAAG ACTTTTTCAG GTGAACATAA CAGACTTGGC CAAGCTAGCA TCTTAGCGGA AGCTGATCTC 008240
008241 CAATGCTCTT CAGTAGGGTC ATGAAGGTTT TTCTTTTCCT GAGAAAACAA CACGTATTGT TTTCTCAGGT TTTGCTTTTT 008320
008321 GGCCTTTTTC TAGCTTAAAA AAAAAAAAAG CAAAAGATGC TGGTGGTTGG CACTCCTGGT TTCCAGGACG GGGTTCAAAT 008400
008401 CCCTGCGGCG TCTTTGCTTT GACTACTAAT CTGTCTTCAG GACTCTTTCT GTATTTCTCC TTTTCTCTGC AGGTGCTAGT 008480
008481 TCTTGGAGTT TTGGGGAGGT GGGAGGTAAC AGCACAATAT CTTTGAACTA TATACATCCT TGATGTATAA TTTGTCAGGA 008560
008561 GCTTGACTTG ATTGTATATT CATATTTACA CGAGAACCTA ATATAACTGC CTTGTCTTTT TCAGGTAATA GCCTGCAGCT 008640
008641 GGTGTTTTGA GAAGCCCTAC TGCTGAAAAC TTAACAATTT TGTGTAATAA AAATGGAGAA GCTCTAAA
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Template:Annotation

Template:Lnc


Annotation (From lncRNAdb)

[ENST00000534336.1]
Section Description
ID Malat1(NR_002819.2)
Characteristics Intergenic ~7kb single exon transcript (Ji (2003), Hutchinson (2007)).
A conserved tRNA-like sequence at the 3' end is cleaved off and processed to generated a short tRNA-like ncRNA mascRNA (MALAT1-associated small cytoplasmic RNA) (Wilusz (2008)).
Post transcriptional processing of Malat1 therefore allows two ncRNAs to be created from the one original transcript (Wilusz (2008)).
Expression Both Malat1 and the processed mascRNA transcript are expressed in a wide range of tissues (Ji (2003), Hutchinson (2007), Wilusz (2008)), Bernard (2010), (Ulitsky (2011)).
Malat1 is highly expressed in the brain. RNA fluorescence in-situ hybridization (RNA-FISH) on adult mouse brain sections showed high expression of nuclear-localized Malat1 transcripts in pyramidal neurons of the hippocampus, Purkinje cells of the cerebellum and neurons of the substantia nigra and motoneurons, but very low levels in non-neuronal cells (Bernard (2010)). In the hippocampus and in Purkinje cells, Malat1 was first detected between post-natal day 0 (P0) and P7 and its level increased until P28 (Bernard (2010)). This high expression appears to come from up-regulation of Malat1 during differentiation, with in-vitro differentiation of neural stem cells showing significant up-regulation of expression in neuronal and glial differentiated progeny (Mercer (2010)).
Expressed in the nucleus accumbens of normal human brains and upregulated in this brain region in heroin abusers (Michelhaugh (2010)).
In neuroblastoma cells Malat1 was up-regulated by the hormone oxytocin (Koshimizu (2010)).
Malat1 is up-regulated in a range of cancers (Ji (2003), Yamada (2006), Lin (2007), Guffanti (2009)).
High expression of Malat1 is associated with metastasis in certain histological subtypes of non-small cell lung cancer (NSCLC) and is predictive of poor prognosis (Ji (2003)).
Malat1 is up-regulated in placenta previa increta/percreta, a disease characterised by excessive invasion of fetal placental trophoblasts into the uterus (Tseng (2009)).
Malat1 is stable in human B cells and Hela and wt MEFs (half-life >7 hrs) but has significantly lower stability in mouse 3T3 and N2A cells. Suggesting differences in Malat1 stability both within and between species (Friedel (2009), Bernard (2010), Clark (2012), Tani (2012)).
Malat1 localises to SC35 domain nuclear speckles in several cell lines (Hutchinson (2007)) (Clemson (2009)). Localisation to nuclear speckles is transcription-dependent, as RNA pol II inhibition promoted re-distribution of Malat1 ncRNA from nuclear speckles to a homogenous nuclear localisation (Bernard (2010)). Malat1 co-localises with pre-mRNA-splicing factor SF2/ASF and CC3 antigen in the nuclear speckles (Bernard (2010)).
MALAT1 is enriched in nuclear speckles in interphase cells and concentrates in mitotic interchromatin granule clusters (IGCs, structural analogs of nuclear speckles present in mitotic cells), but unlike Neat1 it is not required for the structural integrity of the nuclear domain (Tripathi (2010)).
mascRNA derived from Malat1 is transported to the cytoplasm (Wilusz (2008)).
Function Summary: Malat1 has been found to regulate alternative splicing of endogenous target genes, and it is implicated in cancer and a series of molecular and cellular phenotypes, as indicated below.
Identified as an oncogene that promotes tumorigensis. Expression of a Malat1 fragment in NIH 3T3 cells transformed cells (Li (2009)).
Knockdown inhibited cell mobility and lead to decreased expression of several genes (CTHRC1, CCT4, HMMR, or ROD1) that promoted cell migration (Tano (2010)). This result may also explain why knockdown inhibited trophoblast-like cell invasion in-vitro, with MALAT1 hypothesised to regulate the level of trophoblast invasion into the uterus in vivo (Tseng (2009)).
MALAT1 depletion resulted in aberrant mitosis, with a large fraction of cells accumulating at G2/M boundary, and increased cell death (Tripathi (2010)).
Depletion of Malat1 in neuroblastoma cells indicated that Malat1 affects the expression of genes involved not only in the organization and the function of the nucleus, but also in synapse function and dendrite development. In cultured hippocampal neurons, knock-down of Malat1 decreased synaptic density, whereas its over-expression resulted in a cell-autonomous increase in synaptogenesis (Bernard (2010)).
There is a significant enrichment for SRSF1 (SF2/ASF) binding sites within the 5' half of both human and mouse MALAT1, whose direct interaction has been demonstrated, and is dependent on its canonical RRM (RRM1) or the pseudo RRM (RRM2) domains (Sanford (2009), Tripathi (2010)). Independent sequence elements in MALAT1 influence its distribution to nuclear speckles and the recruitment of SRSF1 (Tripathi (2010)).
Additional interactions have been found between MALAT1 and SRSF1, SRSF2, and SRSF3 proteins, but only weak interactions with SRSF5 and PSP1 (an RNA-binding protein that is a component of paraspeckles) have been identified (Tripathi (2010)).
Knock-down of nuclear Malat1 in a transfected U2OS cell line showed that it modulates the recruitment of SR proteins (SRSF1 or SF2/ASF and SC35) to a transcriptionally active transgene array (stably integrated), indicating a role in the regulation of the association of pre-mRNA-splicing factors to transcription sites and control of post-transcriptional gene expression (Bernard (2010)). Malat1 modulates the speckle association of a subset of pre-mRNA splicing factors, such as SF1, U2AF-65, SF3a60, and B-U2snRNP (Tripathi (2010)).
Malat1-depleted HeLa cells show increased cellular levels of dephosphorylated SRSF1 (SF2/ASF) (Bernard (2010)), as well as a moderately increased cytoplasmic pool of poly(A)+ RNA (Tripathi (2010)). It has recently been shown to regulate alternative splicing of endogenous target genes by modulating SR splicing factor phosphorylation, affecting their levels and the distribution and ratio of phosphorylated to dephosphorylated pools (Tripathi (2010)).
Suggested to interact with the PRC2 complex in the HCT-116 cancer cell line (Guil (2012)).
Conservation Therian mammals (found in oppossum as well as placental mammals) (Hutchinson (2007)).
Recently described in zebrafish. Sequence homology to zebrafish was limited to the 3°Ø end, but the ~7kb long, single exon structure as well as positional synteny was conserved, as was the high expression in brain found identified in mammals (Ulitsky (2011)).
Name Malat1: Metastasis-associated lung adenocarcinoma transcript 1.
Neat2: Nuclear enriched abundant transcript 2

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