Difference between revisions of "LINC-ROR"

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LINC-ROR is first found to modulate reprogramming of human induced pluripotent stem cells <ref name="ref1" />.  
 
LINC-ROR is first found to modulate reprogramming of human induced pluripotent stem cells <ref name="ref1" />.  
  
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LINC-ROR is p53 repressor in response to DNA damage <ref name="ref1" />. LINC-ROR can suppress p53 translation through direct interaction with the heterogeneous nuclear ribonucleoprotein I (hnRNP I), and inhibit p53-mediated cell cycle arrest and apoptosis <ref name="ref1" />.  
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LINC-ROR is p53 repressor in response to DNA damage <ref name="ref1" />. LINC-ROR can suppress p53 translation through direct interaction with the heterogeneous nuclear ribonucleoprotein I (hnRNP I), and inhibit p53-mediated cell cycle arrest and apoptosis <ref name="ref2" />.  
  
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Finally, we demonstrate a RoR-p53 autoregulatory feedback loop where p53 transcriptionally induces RoR expression. Together, these results suggest that the RoR-hnRNP I-p53 axis may constitute an additional surveillance network for the cell to better respond to various stresses.
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LINC-ROR also functions as an endogenous miRNA sponge and antagonizes miR-145 to critically regulate the levels of pluripotency transcription factors Oct4, Sox2, and Nanog, in order to ensure embryonic stem cell self-renewal <ref name="ref3" /><ref name="ref4" />.
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RoR can also function as a negative regulator of p53 through interaction with an RNA binding protein, heterogeneous nuclear ribonucleoprotein I. Importantly, a 28-base RoR sequence carrying hnRNP I binding motifs is essential and suffcient for p53 repression. In addition, it can inhibit p53-mediated cell cycle arrest and apoptosis.<ref name="ref2" />
 
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Linc-RoR functions as an endogenous miRNA sponge for differentiation-related miRNAs. and linc-RoR, miRNAs, and the core TFs can form a regulatory circuit consisting of autoregulatory and dualnegative feedback loops during embryonic stem cell (ESC) self-renewal. This regulatory loop maintains a relative balance in self-renewing human embryonic stem cells (hESCs) to resist slight environmental changes and to elicit a rapid response to strong differentiation signals that promote hESCs differentiation. <ref name="ref3" />  
 
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Linc-RoR modulates miR-145 levels, a sits overexpression diminishes endogenous miR-145 in self-renewing hESCs and drastically delays the increase in miR-145 upon hESC differentiation.<ref name="ref4" />  
 
  
 
Linc-RoR can modulate cellular responses during hypoxic stress through modulation of HIF-1a and its downstream targets.<ref name="ref5" />
 
Linc-RoR can modulate cellular responses during hypoxic stress through modulation of HIF-1a and its downstream targets.<ref name="ref5" />
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Linc-RoR and p53 form a RoR-p53 autoregulatory feedback loop where p53 transcriptionally induces RoR expression.<ref name="ref2" />
 
Linc-RoR and p53 form a RoR-p53 autoregulatory feedback loop where p53 transcriptionally induces RoR expression.<ref name="ref2" />
  
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Linc-RoR transcription ias mainly controlled by the core TFs Oct4, Sox2, and Nanog.<ref name="ref3" />
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Linc-RoR transcription is mainly controlled by the core TFs Oct4, Sox2, and Nanog <ref name="ref1" /><ref name="ref3" />.
  
 
===Diseases===
 
===Diseases===

Revision as of 09:49, 31 July 2017

Annotated Information

Name

LINC-ROR:long intergenic non-protein coding RNA, regulator of reprogramming [1]

lincRNA-ST8SIA3 [1]

RoR [2]

Characteristics

The LINC-ROR gene is 2.6 kb in length, located in chromosome 18 (18q21.31), consisting of four exons [2].

Function

A competition for miR-145 between linc-RoR and mRNAs encoding the core TFs[3].

LINC-ROR is first found to modulate reprogramming of human induced pluripotent stem cells [1].

LINC-ROR is p53 repressor in response to DNA damage [1]. LINC-ROR can suppress p53 translation through direct interaction with the heterogeneous nuclear ribonucleoprotein I (hnRNP I), and inhibit p53-mediated cell cycle arrest and apoptosis [2].

LINC-ROR also functions as an endogenous miRNA sponge and antagonizes miR-145 to critically regulate the levels of pluripotency transcription factors Oct4, Sox2, and Nanog, in order to ensure embryonic stem cell self-renewal [4][3].

Linc-RoR can modulate cellular responses during hypoxic stress through modulation of HIF-1a and its downstream targets.[5]

Regulation

Linc-RoR and p53 form a RoR-p53 autoregulatory feedback loop where p53 transcriptionally induces RoR expression.[2]

Linc-RoR transcription is mainly controlled by the core TFs Oct4, Sox2, and Nanog [1][4].

Diseases

malignant liver cancer [5]

Expression

RoR is highly expressed in embryonic stem cells and iPSCs.[2]

In self-renewing human embryonic stem cells (hESCs), linc-RoR is expressed at a high level and removes trace transcribed miRNAs when hESCs are subjected to temporary and slight differentiation agents.[4]

Linc-RoR expression is increased in hypoxic regions within tumor cell xenografts in vivo and is highly expressed in extracellular RNA released by hepatocellular cancer (HCC) cells during hypoxia[5]

Sequence

>NR_048536.1 Homo sapiens long intergenic non-protein coding RNA, regulator of reprogramming (LINC-ROR), long non-coding RNA

000001 GGTGAAATAA ACAGCCATGT TGCTCACACA AAGCCTGTTT GGTGGTCTCT TCACACGGAC GCTCATGAAA TTTGGTGATG 000080
000081 TGACTCGGAT AGGGGGACCT CCCTTGGGAG ATCAGTACCC TGTCCTCCTG CTCTTTGCTC CGTGAGAAAG ATCCACCTAC 000160
000161 AACCTCAGGT CCTTAGACCA ACCAGCCCAA GAAACATCTC ACCAATTTCA AATCCAGACC CCACTGGAAA TCGGACTGTC 000240
000241 CAACTCACCT GACAGCCACT CCCACAGCCG CTGGAACTCT GGCCCAAGGC TCTCTGACTC CTTCCCAGAT CTTCTTGGCT 000320
000321 TAGCGGCTGA AGACTGACGC TGCCCGATCG CCTCGGAAGC CCCCTAGACC ATCACGGACG CCGAGCTTCG GGTAACTCTC 000400
000401 ACAGTGGAAG AAACACAACT ACAGATTTCT ACCTGGTGCA TGGCCATCGC TCATGAAGAC TACAACTTCC AGCTTCCTTT 000480
000481 GAAGAAAAAG AGGACTTGAT GGCATTGTCG CTAAGTAAGA AATAATGTGT GTGACTTCAG GGTTGCCCCC TTAAAGGGAG 000560
000561 GGGACATTTT CCATCCTGCT GTTCAGAGTA TGGATGTGAT GAGAGACATC TTGGATGATG CAGAGGAGGT GAACACCCCA 000640
000641 GGACAATGAA ACCACAGGAG AGAAAGAGCC TGCGCTGGCC CATCTAGCAC AGCCACTGGA CACAGGGACC ACCTGCCTCT 000720
000721 GCACTCTTAT GGAAGGAGGA AATCTAACTT TCCCAGTTTA AGGCACTGTT ACTTTGGGCT CCTGTTACAT AACTGTGGCA 000800
000801 GAATGAAGGT TCAACATGGA AACTGGCAAT GTTGAAGAAA CATAAAGTTC ATTGCTTGAA TATCTGAAGT TGTGGACTCA 000880
000881 ATCTCATACC TGCTCCACTT ATGAGTTATA GTTCTTCCAG GTCTCAGGAA TGGGATCAGC AGGTCTCAGG GTTGTACTCT 000960
000961 CCTGGATCTC TCACCAGCCA CCTCAAACCA GCTGCCATAG CCTGTCCACT TCCACTCCAA TCTTCTCTTC CTTCATCACC 001040
001041 TCCCTTGCAC ACCCTGATAA CCTCGAAAGA GAACTCTTCC CAAGGCTCTG TTCCAAACAC ATCGCCACTC TGCTTAGAAC 001120
001121 CTTCAATGAC TCCTCATGGC CTAGGAGGTT TCTCTCCCAT CTGGATCCAG CTGACGTTCC CAGCACCTTC TCCTGACTCC 001200
001201 TGTCTTTTCT TGAACCAGTT CTGCCCAACA AGGAGGAAAG GGCTGACAGA GTGAAAGTCC CAGGGCATGT GGGAATGTGA 001280
001281 CTCTTTTCAC TTTAAATTCT ATGACTGGAA AGTTTTGGGC AGAGTTGGAC ATGTGCACTT AGCTTCCAGA AGACAGAATC 001360
001361 CTTTTAAAAG AGTCAGAGAA AACACTGGCT TCCTGCCATG ACATGAGATA CAGACAGGAG AGTTGGGAAG CTTTTTAAAG 001440
001441 ATGGCACTAT GACTACAATC ACAGAAACTC TCCATGAGGA AGTAAAAGAA AGCACCTGCA ACACTCCAGC TATGCAGACC 001520
001521 ACTCTGTAAT GGGCTCAGAT CTGGACAGGT GTGTGGAAAG GTGGGTCAAC AGGTCAGGCG TCACAGACTT GGAACATTCA 001600
001601 TGGTGGAAAA GAAAAAGCCC CAAAGAAGAG ACTTCAGGAT AAATGAGAAA ATACTCAAGA CAGCAAAAGT CTCTTTTAGA 001680
001681 AATGTTGGAG AAAGAACACT TAATGTCAGG AGTTACTGTT GATTGATGGC CTTACTGTGT AGCAGGTGAG AAACCCATTG 001760
001761 TTCAGTTCCC TAAAGTCACC CTATTCTCCC AATCATCCTA TGGAGGGGGA ACCATGATGG TTATCCCCAT CTTATAAATA 001840
001841 AAGCAACAGA GGCTTAGAAG GACGAACTCT TTTTCTCAAG GTTACCC