Difference between revisions of "TP73-AS1"

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===Chromosome===
 
===Chromosome===
 
1p36.32
 
1p36.32
 +
 +
===Characteristics ===
 +
[[File:High lncRNA-TP73-AS1 expression in HCC was correlated with poorer prognosis.jpg|right|thumb|High lncRNA-TP73-AS1 expression in HCC was correlated with poorer prognosis<ref name="ref1" />
 +
 +
TP73-AS1, transcribed from chromosome 1p36<ref name="ref1" />.
 +
 +
===Expression===
 +
TP73-AS1 expression was significantly higher in HCC tissues compared to mixed normal tissues<ref name="ref1" />.
 +
 +
RNA sequencing from 11 humans tissues confirmed ubiquitous high expression of 7SK with expression in some tissues being higher than any mRNA ([http://www.ncbi.nlm.nih.gov/pubmed/20668672 (Castle 2010)]).
 +
 +
===Regulation===
 +
In the 7SK ribonucleoprotein, Larp7 binds directly to 3′ terminus of 7SK RNA ([https://www.ncbi.nlm.nih.gov/pubmed/18281698 (Krueger 2008)]) ([https://www.ncbi.nlm.nih.gov/pubmed/18483487 (Markert 2008)]), and prevents degradation of 7SK in vivo ([https://www.ncbi.nlm.nih.gov/pubmed/18281698 (Krueger 2008)]).
 +
 +
===Function===
 +
[[File:Model of hLarp7 recognition of the 7SK.png|right|thumb|Model of hLarp7 recognition of the 7SK 3′end and mechanism of assembly of core 7SK RNP([https://www.ncbi.nlm.nih.gov/pubmed/29946027 (Eichhorn 2018)])]]
 +
 +
7SK snRNA functions in transcriptional regulation by interacting with PTEF-B complex ([http://www.ncbi.nlm.nih.gov/pubmed/11713533 (Nguyen 2001)]) ([http://www.ncbi.nlm.nih.gov/pubmed/11713532 (Yang 2001)]), BAF chromatin-remodeling complex ([https://www.ncbi.nlm.nih.gov/pubmed/26878240 (Flynn 2016)]), or hnRNP R ([https://www.ncbi.nlm.nih.gov/pubmed/29507242 (Briese 2018)]). Consistently, it has been found highly enriched in isolated chromatin fractions, which may be related to its role in transcriptional regulation ([http://www.ncbi.nlm.nih.gov/pubmed/20404130 (Mondal 2010)]). In addition to its critical role for controlling transcription, 7SK snRNA is also involved in alternative splicing ([http://www.ncbi.nlm.nih.gov/pubmed/19416841 (Barboric 2009)]) and the localization of protein in nucleolus ([http://www.ncbi.nlm.nih.gov/pubmed/17381310 (He 2007)]). Therefore, 7SK snRNA has a variety of functions in the nuclear, playing important roles in cell growth and differentiation ([http://www.ncbi.nlm.nih.gov/pubmed/11713533 (Nguyen 2001)]) ([http://www.ncbi.nlm.nih.gov/pubmed/11713532 (Yang 2001)]), axon maintenance ([https://www.ncbi.nlm.nih.gov/pubmed/29507242 (Briese 2018)]) and vertebrate development ([http://www.ncbi.nlm.nih.gov/pubmed/19416841 (Barboric 2009)]).
 +
 +
7SK snRNA controls RNAP II activity by inhibiting P-TEFb elongation factor, which is a cdk-cyclin kinase that functions as both a general and an HIV-1 Tat-specific transcription factor ([http://www.ncbi.nlm.nih.gov/pubmed/11713533 (Nguyen 2001)]) ([http://www.ncbi.nlm.nih.gov/pubmed/11713532 (Yang 2001)]), with an impact on cell growth and differentiation. Specifically, 7SK snRNA functions as the central scaffold that coordinates protein-protein interactions and, by inhibiting P-TEFb kinase-mediated CTD phosphorylation, regulates RNAP II elongation ([http://www.ncbi.nlm.nih.gov/pubmed/11713533 (Nguyen 2001)]).
 +
 +
At an early stage of the HIV transcription cycle, elongation is prevented as P-TEFb is recruited to the HIV-1 promoter in a catalytically inactive state bound to the 7SK snRNP and also the Tat trans-activator of transcription protein. The inhibitory 7SK snRNP may be displaced by the nascent TAR HIV RNA that also binds Tat protein, activating P-TEFb kinase and transcriptional elongation ([http://www.ncbi.nlm.nih.gov/pubmed/20562857 (D'Orso 2010)]). Displacement of 7SK may also be performed by cellular RNAs, as indicated by the 3'-untranslated region (~300-nt) of HIC mRNA, which forms complexes with P-TEFb and is necessary and sufficient for stimulation of P-TEFb-dependent transcription of the HIV promoter ([http://www.ncbi.nlm.nih.gov/pubmed/17925858 (Young 2007)]).
 +
 +
7SK snRNA inhibits enhancer transcription by modulating nucleosome position. 7SK physically interacts with the BAF chromatin-remodeling complex, recruits BAF to enhancers and inhibits enhancer transcription by modulating chromatin structure ([https://www.ncbi.nlm.nih.gov/pubmed/26878240 (Flynn 2016)]).
 +
 +
In axons, 7SK snRNA interacts with hnRNP R to regulate its function in axon maintenance ([https://www.ncbi.nlm.nih.gov/pubmed/29507242 (Briese 2018)]).
 +
 +
7SK snRNP (composed of 7SK snRNA, Hexim1, Larp7/Pip7S, and the P-TEFb subunits CycT1 and Cdk9) is not only critical for controlling transcription, but also for regulating alternative splicing coupled to transcription elongation ([http://www.ncbi.nlm.nih.gov/pubmed/19416841 (Barboric 2009)]).  7SK snRNP disintegration promotes inclusion of an alternative exon via the increased occupancy of P-TEFb, Ser2-phosphorylated (Ser2-P) RNAPII, and the splicing factor SF2/ASF at the minigene ([http://www.ncbi.nlm.nih.gov/pubmed/19416841 (Barboric 2009)]).
 +
 +
7SK snRNA also inhibits APOBEC3C deaminase activity and sequesters it to the nucleolus, suggesting broader role for 7SK RNA in regulating key nuclear functions ([http://www.ncbi.nlm.nih.gov/pubmed/17381310 (He 2007)]).
 +
 +
===Disease===
 +
colon adenocarcinoma <ref name="ref1" />
 +
 +
===Evolution===
 +
Please input evolution information here.
 +
 +
==Labs working on this lncRNA==
 +
Please input related labs here.
 +
 +
==References==
 +
<references>
 +
<ref name="ref1"> Shahriyari L. Effect of normalization methods on the performance of supervised
 +
learning algorithms applied to HTSeq-FPKM-UQ data sets: 7SK RNA expression as a
 +
predictor of survival in patients with colon adenocarcinoma. Brief Bioinform.
 +
2017 Nov 3. doi: 10.1093/bib/bbx153.
 +
</ref>(1)
 +
</references>
  
 
===Disease===
 
===Disease===

Revision as of 08:03, 10 August 2019

Annotated Information

Name

Approved symbol: TP73-AS1

Approved name: TP73 antisense RNA 1

HGNC ID: HGNC:29052

Ensembl ID: ENSG00000227372

Previous names: KIAA0495

Alias symbols: PDAM

Alias names: p53-dependent apoptosis modulator

RefSeq ID: NR_033708

LncBook ID: HSALNT0289273

Chromosome

1p36.32

Characteristics

[[File:High lncRNA-TP73-AS1 expression in HCC was correlated with poorer prognosis.jpg|right|thumb|High lncRNA-TP73-AS1 expression in HCC was correlated with poorer prognosis[1]

TP73-AS1, transcribed from chromosome 1p36[1].

Expression

TP73-AS1 expression was significantly higher in HCC tissues compared to mixed normal tissues[1].

RNA sequencing from 11 humans tissues confirmed ubiquitous high expression of 7SK with expression in some tissues being higher than any mRNA ((Castle 2010)).

Regulation

In the 7SK ribonucleoprotein, Larp7 binds directly to 3′ terminus of 7SK RNA ((Krueger 2008)) ((Markert 2008)), and prevents degradation of 7SK in vivo ((Krueger 2008)).

Function

Model of hLarp7 recognition of the 7SK 3′end and mechanism of assembly of core 7SK RNP((Eichhorn 2018))

7SK snRNA functions in transcriptional regulation by interacting with PTEF-B complex ((Nguyen 2001)) ((Yang 2001)), BAF chromatin-remodeling complex ((Flynn 2016)), or hnRNP R ((Briese 2018)). Consistently, it has been found highly enriched in isolated chromatin fractions, which may be related to its role in transcriptional regulation ((Mondal 2010)). In addition to its critical role for controlling transcription, 7SK snRNA is also involved in alternative splicing ((Barboric 2009)) and the localization of protein in nucleolus ((He 2007)). Therefore, 7SK snRNA has a variety of functions in the nuclear, playing important roles in cell growth and differentiation ((Nguyen 2001)) ((Yang 2001)), axon maintenance ((Briese 2018)) and vertebrate development ((Barboric 2009)).

7SK snRNA controls RNAP II activity by inhibiting P-TEFb elongation factor, which is a cdk-cyclin kinase that functions as both a general and an HIV-1 Tat-specific transcription factor ((Nguyen 2001)) ((Yang 2001)), with an impact on cell growth and differentiation. Specifically, 7SK snRNA functions as the central scaffold that coordinates protein-protein interactions and, by inhibiting P-TEFb kinase-mediated CTD phosphorylation, regulates RNAP II elongation ((Nguyen 2001)).

At an early stage of the HIV transcription cycle, elongation is prevented as P-TEFb is recruited to the HIV-1 promoter in a catalytically inactive state bound to the 7SK snRNP and also the Tat trans-activator of transcription protein. The inhibitory 7SK snRNP may be displaced by the nascent TAR HIV RNA that also binds Tat protein, activating P-TEFb kinase and transcriptional elongation ((D'Orso 2010)). Displacement of 7SK may also be performed by cellular RNAs, as indicated by the 3'-untranslated region (~300-nt) of HIC mRNA, which forms complexes with P-TEFb and is necessary and sufficient for stimulation of P-TEFb-dependent transcription of the HIV promoter ((Young 2007)).

7SK snRNA inhibits enhancer transcription by modulating nucleosome position. 7SK physically interacts with the BAF chromatin-remodeling complex, recruits BAF to enhancers and inhibits enhancer transcription by modulating chromatin structure ((Flynn 2016)).

In axons, 7SK snRNA interacts with hnRNP R to regulate its function in axon maintenance ((Briese 2018)).

7SK snRNP (composed of 7SK snRNA, Hexim1, Larp7/Pip7S, and the P-TEFb subunits CycT1 and Cdk9) is not only critical for controlling transcription, but also for regulating alternative splicing coupled to transcription elongation ((Barboric 2009)). 7SK snRNP disintegration promotes inclusion of an alternative exon via the increased occupancy of P-TEFb, Ser2-phosphorylated (Ser2-P) RNAPII, and the splicing factor SF2/ASF at the minigene ((Barboric 2009)).

7SK snRNA also inhibits APOBEC3C deaminase activity and sequesters it to the nucleolus, suggesting broader role for 7SK RNA in regulating key nuclear functions ((He 2007)).

Disease

colon adenocarcinoma [1]

Evolution

Please input evolution information here.

Labs working on this lncRNA

Please input related labs here.

References

  1. 1.0 1.1 1.2 1.3 Shahriyari L. Effect of normalization methods on the performance of supervised learning algorithms applied to HTSeq-FPKM-UQ data sets: 7SK RNA expression as a predictor of survival in patients with colon adenocarcinoma. Brief Bioinform. 2017 Nov 3. doi: 10.1093/bib/bbx153.

Disease

esophageal squamous cell carcinoma.

pubmed IDs

9455484, 20477830, 23726844

Sequence

>gi|297747264|ref|NR_033708.1| Homo sapiens TP73 antisense RNA 1 (TP73-AS1), transcript variant 4, long non-coding RNA

000001 GTTGTTGCGG GATCTCACAG GCTTTAAACC GCGGCGCCGC GGCGCCCGGG TGTGGATCCC TAGATGGGAG CCGGGGATGG 000080
000081 GCCGGGTGCC TGGTGGGTGG CAGTCGGGGC TGACGGCGGC GGCACTTTGC CGCCTCAGGC CCTGGACACC TTCACCCCGC 000160
000161 CGCCTGCCCA GGCGGGCCGG CCCTGCCCGT CCACCGGCCG CCGAGAGTCC CCGGCCTTGG GTCCCCGGGG CCGCTGACTG 000240
000241 GCCTCGGTCA CCTCCCGGGG AAGGCTCCCG CGCCTCCATC TGCCCCCGCA GGAAGGGACC CTCTTCTCGC CCGCGAGGCT 000320
000321 TCTCCGGGTG GGATCGTCCT GGCCCCCAGC CCTAAGGGAT CCGCCCCCTC CGAGCATCCG CCGCCCCTCG GAGACCACTC 000400
000401 CAGCTCGGAC GGACCCACTC CAGCCCCCGC TGCACGCGGA AGCGCTCATC CTCCCCGCCT GCCCCGTTCC CTCCCCCTTC 000480
000481 TCCTGTGGGA CAACCAGGGA CCGCAGCTCC CCGCTCCCCA GGTGTGGGGG CTCCGACACG AACGCCTCTG CTCGCAGGGC 000560
000561 GGTGAGCGCA GATCCCACGG GTCCCTCGGT CGGGGGTCGA GGCTGCTTCC GTTTCCATCC CGGACCCGAC AATGGGCGGG 000640
000641 AAAAAGAAGG CTTTACACGA CTACGCGGCG GAGTTCACCG ACCTGGTGGT GAAGCACCTG ATTGAGCACA GTGACTCTGG 000720
000721 GGACACGTCT GTGGTGGAGA CCCTTTACTG CAGGGCCTGC GAGCTGCCCG TGCGCGTGCG GAGGGACCGC ATCCTGGAAC 000800
000801 ACCTGTCCTC GGGCAGGCAG CACGGCCTGC GGACGCCCAT TCTCATGTAA ATGTCAGTGC CAACGCTGGT GTTTCAGGAG 000880
000881 TCATCCCAGC GGGCTGCGGG CTATTTTAGG ATTCTCTGCC CTGCAAACGT TTCCAAAGTA CGTGGACAGG CCGCCTGATG 000960
000961 ACACTACGTT TACGGGATCT GCTAGTGGCT TGCCTACTTA GGGAGTAAAC CCTGTGAAGT CTCGCAGTTT TGTTAAAGTG 001040
001041 TGCGTGGCCA CCTGAATGCT GCCTTATCAC AAGCCAGATA CATACTGGTC TGTAGGGTAA CTCCCCACTG TTGATCCTCT 001120
001121 GAGATGATTG TGGACTGGGT GCTGTGAGTC CTGCCACTTT GTTTAAGTGA ATGTGTCTTT TGTCCAGCTC AGCCGCCTCG 001200
001201 GATCTCGCTG CCACCAGCCT TACTGCACAC CCGTGCCACC CGCCCTTGCC CCGTCAGCCT CAGCCTCAGC TCATTCTCTC 001280
001281 AGGCAGTCCC AGCATTGGCA CGGTACCTCC TCCCGCTGTG GGCCACACGT CTCTGCTCCC TGTCAACCCT CCTGCCATCA 001360
001361 GCACCACCAC CAGCGACTTG TCTGCCCGGG AGGATGCAAC ACCATCTGCC TCCACCGGCC ACCTTTCAGT GTTTCCTGCT 001440
001441 TTCCAAGTAA AGATACCAGC AGTGCCCTCA GAGCAGACCA GCCAGAGTTT TTCTGAAGCC TCCCACAGGG TGCTCCCCGG 001520
001521 AGGAGGCCCG AGATGCTCTC GTGACTTTGG AGCCGGGGTG GCTGGCCACC TTGGCCTGGG CATCTTTGGG GTGGGCTTCG 001600
001601 GGAGCCCGGC ACTGCTGCAG AGTGTGGTGG ATGAGAACAG CTGCTGCTTG CTGTACGTGG TGGAGGACCA GCTGTGTGAT 001680
001681 GTGGAGCAAG CCTTCAGAGC TGAGCATTTG GGCCAACACC AGAGTGGTTC GGGAACAGGA TGCAGACATT GTCCTCAACG 001760
001761 ACCAGCGGCA CTTTGATCCG GTTTTCCAGT TCTTGCACAA GCAAGTTTGT GTCAGCCACG CCCTGGGGAG GATCCACTGG 001840
001841 ATCACCGCCG TCACTGCCTG TTCCCGGCGG CCTCTCCGGC TTCCCTAAAG AGAGCAGCTT CCCTCGAGAC CAGAAGCCAG 001920
001921 AGCTCACCCT CCCTTGTGTC CAGGTGGGAC TTTCTACAAC GCTGCTGTGC ACGACGTGGA TGCCGTATGC ATGTTGCTGG 002000
002001 GGGAAGCCAC TCCGGACACT GTGTTTTCTC TGGGACATGT CTTCTGCCCA GATATGGCCG CCTTAAAAGA TGCAGATGCT 002080
002081 GTTGTGATCA GCATGAAGTT TCCCTGTGAG GCCGTGGTTA GCGTGGACAT CAGCCAGCAC TGCACAGACA GCTGCGACCA 002160
002161 GGACGTCAGC CAGCACTGCA CAGACAGCTG CGACCAGAGA CTGGAGATGG AGTCTTGCCC TGTCACCCAG GCTGGAGTGC 002240
002241 AATGGTGCGA TCTCGGCTCA CTGCAACCTC CGTCTCCCAG GTTCAAGCGA TTCTTCTGCC TCAGCCTTCT GAGTAGCTGG 002320
002321 GATTACACGC GTGTGCCACC ACGCTCGGCT AATTTTTGTA TTTTTAGTAG AGATGGGATT TCACCATGTT GGCCAGGCTG 002400
002401 GTCTCGAACT ACTGACCTCG TGATCCACCT GCCATGGCCT CCCAAAGTGC TGGGATTACA GGCGTGAGCC ACCATGCTCG 002480
002481 GCCTAAAAAA CAATTTTCTT GAAGAATCCG ATTTTGTGCA TAGTAATGAC ACAGCACCAT TCCTGAGAAA TAGGAAATAT 002560
002561 ATGTGTGTGG TATGAAAAGC CCATATTCTG TTCTTGTCAC CTGAATCTAG GCTTCCTCTT TGGATGTGAA CGCGGGAATG 002640
002641 AACAGTGGCT GTTTTCCACC CAAAGGGGCG TGGAGACCTT TTGGAAACGG GCTTTCTCCT TTCCATTTTG CAGCCGGGGG 002720
002721 CGGGTGGAAA CCTTCCTTCG AAGGGTAGTG CCTTGGGGAG CAGCAGACCT GCTCTGAGTC CAGCTTAGCT TTCCAAAATT 002800
002801 CTGTGTGGAA CTTACTGGAG ATGTTTTTAT ATATTTGAAA ATAATGGCCT GTATTTCTCA CGCTATACTT AAAAAAAATA 002880
002881 ACTAACCTTT TAAACAAAGA TATTCAAACT CACCCTTGTG CTGAAAGCAC TCACATTTCT GTGTTCATTC CTGAAAGGGC 002960
002961 GTTTTAGAGT CCCCGTTTCT ACGTTCTATG TGGCACCCTC TTGCCGAGGG AACATCCAGA ATCCCTCCAC TTCCTGTCTA 003040
003041 GTTTGAGGCC TCAACACCTT CATGATCCAG AGTCCTGCGG CTATGAGGGG GTGGGCCCAC CACCGCCCAG CCCTCCTTGG 003120
003121 TGGACGTGGG GACAGGTAGG AGCCTAGGGA AAGGGGTGGG CGGGCTCTGG TGTGACGGCG TGAGCGCTAG CCAGGAAGAT 003200
003201 GGGGCCAGGG CTTGGCATGG CACCTCACCT GTGGGGGAAC TCGGCGGAGC TTCCTGGCGG CATCTCCCCC TCTTGCCTTG 003280
003281 GTCCTTTCTA TCTTTGTTTT AGGCCAATTT CTAAAAAGAC TGAGGCCTCC TTCAAGGTTG AACAGATTTC TAGAGCCTTG 003360
003361 TTTTTGCTGT GACAAGTCCC TAGTCCCTGT TCACAACTCT GAAACCAAGA AACCTGAGAA CCAAGAGAAC TGAAATGAAG 003440
003441 CCCGTTGGTC TCAGCCTGGC TTGAGCCAAC ATGAGGCTCT CTGCTGCCTT TTGTTTTCTT AGGTTTTGCT GAGAAACGGG 003520
003521 AGTGCGTTCT GTGTCGGTGT TTGTGACGCC CTGAGACCCT GCTTGGCCTA GCTAAAGTCC AGAAGGCCTG GGCCCCACAG 003600
003601 GGCTTGGATG AGGGCTCATG GGCCTGTACT TCAGGAGGCC TGAGAGGCCC GGTCAGTCCC ATGAGGCTAC TCGGCTTGGC 003680
003681 CCGCAGGTCC TCCGAGGCAC AGGGCAGAGG GACACCCCAG GGACCCATCA GACTCACGAC ACAGAGAAAC TCAAGTGGGG 003760
003761 TGCCAGGGCC GGCCACAGAG GCCACGGGCT TCCTGCCTGT GAGGAGCCGC CCTGTTTGTC TGAGCCCTTT GGAGATTTAG 003840
003841 GTTGAGTCAT GAGAACCGGT CATTGGAACA TACACTTTAT TATGTTACAA AAACAAAAAT CCCCACTGAA ACACAGCTAA 003920
003921 AAAAATAACA CATTTTCCCA AGATTACATT ACCAAAAACA GTTGTTATGT CATTGGAGGG CGTCCATTAA TACTGCTCGG 004000
004001 AGAAGCACGA TCTTACACGA AAAACACGGA TGGGATTTCG TTTTCACCTT AAAGCATTAA AGTGCTTTAA CTGGTAA