Difference between revisions of "LINC00470"

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LncBook ID: [https://bigd.big.ac.cn/lncbook/transcript?transid=HSALNT0246856 HSALNT0246856]
 
LncBook ID: [https://bigd.big.ac.cn/lncbook/transcript?transid=HSALNT0246856 HSALNT0246856]
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===Chromosome===
 
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18p11.32
 
  
 
===Characteristics ===
 
===Characteristics ===
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[[File:Functional domains of 7SK RNA..png|right|thumb|Functional domains of 7SK RNA([https://www.ncbi.nlm.nih.gov/pubmed/19246988 (Diribarne 2009)])]]
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[[File:LINC00470 positively regulated the pAKT level.jpg|right|thumb|LINC00470 positively regulated the pAKT level<ref name="ref1" />.]]
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~330 nt in vertebrates*. Transcribed by RNAP III, GC-rich sequence forming conserved secondary structures (especially 3' and 5' stem-loop motifs).
 
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The 7SK gene is located on chromosome 6, and chromosome 6 is the sole human chromosome that produces 7SK RNA ([https://www.ncbi.nlm.nih.gov/pubmed/8139910 (Driscoll 1994)])
 
  
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7SK RNA is capped at its 5' end by BCDIN3, a specific methylase methylphosphate capping enzyme (MePCE) ([http://www.ncbi.nlm.nih.gov/pubmed/17643375 (Jeronimo 2007)]).
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LINC00470 (also known as C18orf2) is a long non-coding RNA located in chromosome band 18p11.32 between RP11-16P11 and RP11-732L14, Its alternative splicing of seven exons generates four transcripts<ref name="ref1" />.
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RNAP II was recently found to bind near 7SK promoter, as well as many other known Pol III genes, suggesting that RNAP II may also play a role in regulating their transcription ([http://www.ncbi.nlm.nih.gov/pubmed/20139302 (Raha 2010)]).
 
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In invertebrates, 7SK homologs may have different sizes (such as >400 nt and ~130 nt in drosophilids and nematodes, respectively). ([http://www.ncbi.nlm.nih.gov/pubmed/20139302 (Gruber 2008)]) ([http://www.ncbi.nlm.nih.gov/pubmed/18566019 (Marz 2009)])
 
  
 
===Expression===
 
===Expression===
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Nuclear, highly abundant (one of the most abundant small RNAs in vertebrate cells), first isolated from HeLa nuclear extracts, but ubiquitously expressed.
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LINC00470 expression levels in astrocytoma were significantly higher than those in normal brain tissues, high expressed in GBM<ref name="ref1" />.
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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===
 
===Regulation===
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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)]).
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Please input regulation here.
  
 
===Function===
 
===Function===
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[[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)])]]
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[[File:LINC00470 inhibited HK1 ubiquitination to affect glycolysis by positively regulating AKT activation.jpg|right|thumb|LINC00470 inhibited HK1 ubiquitination to affect glycolysis by positively regulating AKT activation<ref name="ref1" />.]]
  
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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)]).  
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LINC00470 was a positive regulator for AKT activation in GBM. LINC00470 bound to FUS and AKT to form a ternary complex, anchoring FUS in the cytoplasm to increase AKT activity. Higher pAKT activated by LINC00470 inhibited ubiquitination of HK1, which affected glycolysis, and inhibited cell autophagy<ref name="ref1" />.
  
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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)]).
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===Disease===
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astrocytoma <ref name="ref1" />
  
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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)]).
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GBM<ref name="ref1" />
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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)]).
 
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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)]).
 
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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)]).
 
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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)]).
 
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===Disease===
 
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colon adenocarcinoma <ref name="ref1" />
 
  
 
===Evolution===
 
===Evolution===
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==Labs working on this lncRNA==
 
==Labs working on this lncRNA==
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Please input related labs here.
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* Hunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha, 410006, Hunan, China.
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* Cancer Research Institute, School of Basic Medical Science, Central South University, Changsha, 410078, Hunan, China.
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* Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha, 410078, Hunan, China.
  
 
==References==
 
==References==
 
<references>
 
<references>
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<ref name="ref1"> Shahriyari L. Effect of normalization methods on the performance of supervised
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<ref name="ref1"> Liu C, Zhang Y, She X, et al. A cytoplasmic long noncoding RNA LINC00470 as a new AKT activator to mediate glioblastoma cell autophagy[J]. J Hematol Oncol, 2018, 11: 77.
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learning algorithms applied to HTSeq-FPKM-UQ data sets: 7SK RNA expression as a
 
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predictor of survival in patients with colon adenocarcinoma. Brief Bioinform.
 
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2017 Nov 3. doi: 10.1093/bib/bbx153.
 
 
</ref>(1)
 
</ref>(1)
 
</references>
 
</references>

Latest revision as of 12:40, 11 August 2019

Annotated Information

Name

Approved symbol: LINC00470

Approved name: long intergenic non-protein coding RNA 470

HGNC ID: HGNC:1225

Previous names: chromosome 18 open reading frame 2

Previous symbols: C18orf2

RefSeq ID: NR_023925

Ensembl ID: ENSG00000132204

LncBook ID: HSALNT0246856

Characteristics

LINC00470 positively regulated the pAKT level[1].

LINC00470 (also known as C18orf2) is a long non-coding RNA located in chromosome band 18p11.32 between RP11-16P11 and RP11-732L14, Its alternative splicing of seven exons generates four transcripts[1].

Expression

LINC00470 expression levels in astrocytoma were significantly higher than those in normal brain tissues, high expressed in GBM[1].

Regulation

Please input regulation here.

Function

LINC00470 inhibited HK1 ubiquitination to affect glycolysis by positively regulating AKT activation[1].

LINC00470 was a positive regulator for AKT activation in GBM. LINC00470 bound to FUS and AKT to form a ternary complex, anchoring FUS in the cytoplasm to increase AKT activity. Higher pAKT activated by LINC00470 inhibited ubiquitination of HK1, which affected glycolysis, and inhibited cell autophagy[1].

Disease

astrocytoma [1]

GBM[1]

Evolution

Please input evolution information here.

Labs working on this lncRNA

  • Hunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha, 410006, Hunan, China.
  • Cancer Research Institute, School of Basic Medical Science, Central South University, Changsha, 410078, Hunan, China.
  • Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha, 410078, Hunan, China.

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Liu C, Zhang Y, She X, et al. A cytoplasmic long noncoding RNA LINC00470 as a new AKT activator to mediate glioblastoma cell autophagy[J]. J Hematol Oncol, 2018, 11: 77.

Sequence

>gi|193083199|ref|NR_023925.1| Homo sapiens long intergenic non-protein coding RNA 470 (LINC00470), transcript variant 1, long non-coding RNA

000001 AATGCCTTAA AGAAAGGACT GATCTCCCCT GAAGAAGAGA GAATTCTGCC TCTAGATTGC TTACAATTTG AACTGGAACA 000080
000081 TCAGCTGTTC TCTAGGTCTT AAGTCTGCTG CTCTAACCTA CAAATTTTGG ACATGCCAAT CTCCACAGTC ACATGGGCCA 000160
000161 ATTCCTTAGT TTCTCTGGAG AATCCTGACT AATGTATGCA ATGTCTTTAT TTCATCCTCA TTCTTAAAGG ATATTTTCAT 000240
000241 CAGCAACACC ACACCCTCCT GATCACCATA GCTTTATGAT CTGAGCTTTC ATCTGGTATC ATTTCCTTTC CGTCTGAAGA 000320
000321 ACTTGCTTTC CTTGCAACAA CAAGAAACAA ATTTATTAGC TAACCTAACC ACTAATGACG CAAGAGACAA TTCTAAGGAC 000400
000401 TTTCAAAACA GCAAAGTAGG AGCAGCTGCT ACCTCTAGGG ATGAGGGAGA AACTCAAAAA TGCATACAAA AACCATTGCA 000480
000481 TGAAAAGTGA CTGGATTTGT ACATAGCGTC AGGAGATGTG CGTAGTGTCA AAGTATCTCA TCACACATTA CTTGATAATT 000560
000561 ACAAATGAGA AAAATGAACC TTCACAGTGG CAAGACTTGA CTTCTACCTC TTTCAAAAAG ATGCAATTGT CCAATTATTG 000640
000641 GTGAAATTGT CATTTCATGC TATTGGCTAT TTGAAATTCC TCCTCTAATT TCAGAATAAA TCACTGAAAT TGACATCGGC 000720
000721 CAGTCTGAAT TTCAAGAAAT TACCTGCTGA AGACAAGAGG GATCTCTTCT TCAGATTTGC AGTCTGGGGA AGACACAGCC 000800
000801 TCTACTGTAC TTTAGAACCT GAGATATGGT GGTGGAGGGA GCCCTGGGTC GAGTGGTAAG ATTCACCCTT AGGTTAGTAT 000880
000881 TGACGTAAGG TGACGAGGAG CTGTAGACAA AAGATTGTAA CCATAAGAAC TTCATAGTTT TTGTATTTTC ACCGAGCTTA 000960
000961 TATTTGGTGT GTTTTTTGTC TTTTCTTTAT GATTATCAAT AAAATGCTTG AAAGGAGATG AGGTTGGGGA ATAATTTTTG 001040
001041 GGAATACCAC AAAAGACACT TTTGTGATGG AAATCCTTAA AAAGACACAA TCCATTACCT CATTGGGTTC AAAAGGCAAT 001120
001121 TGTGAACTAC TGTGGAGTTT GGAAAGAAGC AATGAGGTAA TCAAGGATAC TGTTGACAAT CTAGCTTATC CTATGGATGG 001200
001201 AAGGAAATTG AAACTAATGG AGGCGAGGCT GGTAAAACAA TAGGGTTTGA GACAATTCTG TGGCATTAGA AATGAAAGAG 001280
001281 GAAGGTGAAT CCGGGAGACG GAGCTTGCAG TGAGCTGAGA TCGCGCCACT GCACTCCAGC CTGGGCGACA GAGCGAGACT 001360
001361 CCATCTCAAA AAAAAAAAAA AAGAAAGAAA GAAAAGAAAG AGGAAGTAAT AATCTGTGAA ATTTTTCCTT AGGAACTTAT 001440
001441 TGGCAATTTA AAAATGAATT TGTTAAGCCA TGCTGGTTCT GACCCAAAAG CCATTCCCCA GCCTTCCTCA CTCCCCTCTT 001520
001521 TCACTACTGG CAGAGATTGT CTCTCATTTT ACAAGCTGAA AATGCCAGAT GCTTGCTTTT ACAGTCTTCC TTACACCCAG 001600
001601 AGCATGTGCA TATGTTTAAA CGGTCAAGAA GAAGTCATAA CATGGGTGTC TGGGAGAGCT TTTATCCCAC AAAAACAACA 001680
001681 CTTCACTCAA AAAACAAACC AAACAAAGAA AAATTCTCCT TCCTGCCATT GGATGTGAGG CTCAGACCTC TAGTAACCAT 001760
001761 TTTGTGACCA CAAAGCAACA AGCCTGAGGA AAAGTCCTAC ACGCTGAGCA ACAGGCAGAA ATATTGCCAT CGCTGAGTTG 001840
001841 CAGAAACAAA TCTAGAGATG TTTTGCTTCT GTAATTATTT TTTATGGGAG ATTACAAGTG GGTTTACTGT TCACTTTTCA 001920
001921 AATCTTATTT CTCTATGATG TTTAGCTTGG GTAAATTTTA CCTTAAATCC ACTTTTTTAT GTAAGGTAAC ATATTTGTCG 002000
002001 GTTTCAAGGA TTAAGATGTG GGCATACTTG GAGGCCATTA TTTTGCCCAC CACAGGTGAA AAAGGAAGTG TTATTCTTAA 002080
002081 ATCATTTGGA AGGATCTCTG TGTAAATGCA AGAGCGAGAC AAGAAAATGC TGTCATTCTT TTGATATGGA CTCGAATTTC 002160
002161 CACTTCATGG TTGTCTGCTT CCTTTTTAGA GTATTATTTA TCCTCCTAAT AAAAAGAAAG TGAAATTTCC C

Predicted Small Protein

Name LINC00470_smProtein_1883:2104
Length 73
Molecular weight 8461.072
Aromaticity 0.191780821918
Instability index 13.9932876712
Isoelectric point 9.65484619141
Runs 13
Runs residual 0.0339372514361
Runs probability 0.0446713682008
Amino acid sequence MGDYKWVYCSLFKSYFSMMFSLGKFYLKSTFLCKVTYLSVSRIKMWAYLEAIILPTTGEK
GSVILKSFGRISV
Secondary structure LLLEEEEEHHHHHHHHHHHHHHLHHHEEEEEEEEEEEEEHHHHHHHHHHHHHEELLLLLL
LEEEEELLLEEEL
PRMN LLLLLLLLLLLLLLLLLLLLLLLLLLLLLHHHHHHHHHHHHHHHHHHLLLLLLLLLLLLL
LLLLLLLLLLLLL
PiMo iiiiiiiiiiiiiiiiiiiiiiiiiiiiiTTTTTTTTTTTTTTTTTTooooooooooooo
ooooooooooooo
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