Difference between revisions of "NONHSAT121673"
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===Diseases=== | ===Diseases=== | ||
− | [[File: The implication of APTR-mediated p21 silencing in normal cell function and cancer.jpeg|right|thumb| | + | [[File: The implication of APTR-mediated p21 silencing in normal cell function and cancer.jpeg|right|thumb|300px|'''The implication of APTR-mediated p21 silencing in normal cell function and cancer''' <ref name="ref1" />.]] |
* Glioblastomas<ref name="ref1" /> | * Glioblastomas<ref name="ref1" /> | ||
===Function=== | ===Function=== | ||
− | [[File:LncRNA APTR knockdown inhibits cell proliferation in a p53-independent manner.jpg|right|thumb| | + | [[File:LncRNA APTR knockdown inhibits cell proliferation in a p53-independent manner.jpg|right|thumb|300px|'''LncRNA APTR knockdown inhibits cell proliferation in a p53-independent manner'''<ref name="ref1" />]] |
The 3' portion of ''APTR'' specifically interacts with and recruits the PRC2 protein complexes EZH2 and SUZ12 to repress P21 promoter specifically between −1.6 to −4 kb relative to the TSS, which requires the c-Alu elment of APTR.<ref name="ref1" />. | The 3' portion of ''APTR'' specifically interacts with and recruits the PRC2 protein complexes EZH2 and SUZ12 to repress P21 promoter specifically between −1.6 to −4 kb relative to the TSS, which requires the c-Alu elment of APTR.<ref name="ref1" />. | ||
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APTR as a new member of TGF-β1-dependent ncRNAs that are involved in liver fibrosis. <ref name="ref2" /> | APTR as a new member of TGF-β1-dependent ncRNAs that are involved in liver fibrosis. <ref name="ref2" /> | ||
===Expression=== | ===Expression=== | ||
− | [[File: Expression of APTR in fibrotic liver tissues and activated HSCs.jpg|right|thumb| | + | [[File: Expression of APTR in fibrotic liver tissues and activated HSCs.jpg|right|thumb|300px|'''Expression of APTR in fibrotic liver tissues and activated HSCs.''' <ref name="ref2" />.]] |
''APTR'' is a capped, poly(A) tailed and spliced lncRNA expressed mainly in nucleoplasm (Figure 1F) and required for proliferation of multiple cell-lines. <ref name="ref1" /> | ''APTR'' is a capped, poly(A) tailed and spliced lncRNA expressed mainly in nucleoplasm (Figure 1F) and required for proliferation of multiple cell-lines. <ref name="ref1" /> | ||
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| | 5' -GGGCTCAGAGAAGTCTGGTG-' <ref name="ref1" /> | | | 5' -GGGCTCAGAGAAGTCTGGTG-' <ref name="ref1" /> | ||
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| | 5'- UACAAACACCGCUAGUGGCdTdT -3'<ref name="ref2" /> | | | 5'- UACAAACACCGCUAGUGGCdTdT -3'<ref name="ref2" /> | ||
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==Labs working on this lncRNA== | ==Labs working on this lncRNA== |
Latest revision as of 11:08, 30 June 2017
APTR,a 2303-nucleotides lncRNA, acts in trans to repress the CDKN1A/p21 promoter by recruiting PRC2, which requires a complementary-Alu sequence encoded in APTR for the localization of APTR.
Contents
Annotated Information
Name
APTR: Alu-mediated CDKN1A/p21 transcriptional regulator (non-protein coding)
RSBN1L-AS1:RSBN1L antisense RNA 1 (non-protein coding)[1]
Characteristics
APTR is a 2303-nucleotides lncRNA which expressed from the opposite strand of the intergenic region between PTPN12 and RSBN1L in chromosome 7q21 possesses two sequences complementary to SINE/Alu elements (c-Alu) as well as one sequence complementary to LINE/L2 element[1].
Cellular Localization
- Nucleoplasm[1]
Diseases
- Glioblastomas[1]
Function
The 3' portion of APTR specifically interacts with and recruits the PRC2 protein complexes EZH2 and SUZ12 to repress P21 promoter specifically between −1.6 to −4 kb relative to the TSS, which requires the c-Alu elment of APTR.[1].
The level of expression of APTR is important for determining the expression of p21 in GBM cell lines and tumors[1].
APTR can accelerate cell cycle and increase the proliferation of HSCs via negatively regulating p21 in mouse liver fibrosis. [2]
APTR as a new member of TGF-β1-dependent ncRNAs that are involved in liver fibrosis. [2]
Expression
APTR is a capped, poly(A) tailed and spliced lncRNA expressed mainly in nucleoplasm (Figure 1F) and required for proliferation of multiple cell-lines. [1]
APTR expression is upregulated in liver fibrosis. [2].
Experiment | Primer | Forward primer | Reverse primer |
---|---|---|---|
RT-PCR | APTR 650-950 Primer set1 | 5’-TGTGGGTACAAAAGGAGAGTAACAT-3’ | 5’-GTAGATCTGGAGCTGCAACTACAG-3’[1] |
APTR 1832-2158 Primer set 2 | 5’-GAGGAAGAGAAATTCTGAGGGTAAAGATA-3’ | 5’-GATCTGTGCATCACTCTATTCATCCATT-3’[1] | |
Knockdown | siAPTR#1 | 5'-CCAGGUACUGCCUUCUAAC-3'[1] | - |
siAPTR#2 | 5'-CCAUGAUCCGGUAUCACCA-3'[1] | - | |
ChIP/CLIP | Region 1 | 5’-GAGGTCGAGGTTTGAGACCAGCCT-3’ | 5’-GTGTGCACGTAACAGAGCGCATCA-3’[1] |
Region 2 | 5’-GTCTGCTGCAAATCTCAGTTTGCCC-3’ | 5'-TTATCTCGAGCAGGAAAACGTGGTCTCAGC-3'[1] | |
Region 3 | 5’-CAGATTTGTGATGCTAGGAACATGA-3’ | 5’-AGAGGCGGAACAAAGATAGAACATT-3’[1] | |
Region 4 | 5’-TATGCTGCCTGCTTCCCACCAACA-3’ | 5’-TTCCTCACCTGAAAACAGGCAGCC-3’[1] | |
Region 5 | 5’-GAGTCAGATTCTGTGTGTGAC-3’ | 5’-ATAACTTCTAGCTCACCACCACCAC-3’[1] | |
Region 6 | 5’-GGCCTTTCTGGGGTTTAGCCACAA-3’ | 5’-CTTCTTCCTCTAACGCAGCTGACCTC-3’[1] | |
Region 7 | 5' -TTGTCATTTTGGAGCCACAG-3' | 5' -GGGCTCAGAGAAGTCTGGTG-' [1] |
Experiment | Primer | Forward primer | Reverse primer |
---|---|---|---|
qRT-PCR | APTR | 5’- TTGCCAAACGGTTCTTTC-3’ | 5’- CGGAGGAGAGTAAATACAACAG -3’[2] |
Knockdown | siRNA1 | 5'- GUGCAUCAGUGUUGCUUGCdTdT -3' | 5'- GCAAGCAACACUGAUGCACdTdT -3'[2] |
siRNA2 | 5'- GGCGAAACCGACACCGAAAdTdT -3' | 5'-UUUCGGUGUCGGUUUCGCCdTdT -3'[2] | |
siRNA3 | 5'- GCCACUAGCGGUGUUUGUAdTdT -3' | 5'- UACAAACACCGCUAGUGGCdTdT -3'[2] |
Labs working on this lncRNA
- Department of Biochemistry and Molecular Genetics, University of Virginia School of Medicine, Charlottesville, Virginia, United States of America. [1]
- Department of Gastroenterology, Jinshan Hospital of Fudan University, Jinshan, Shanghai, 201508, China [2]
References
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 Negishi, M. et al. A new lncRNA, APTR, associates with and represses the CDKN1A/p21 promoter by recruiting polycomb proteins. PLoS One 9, e95216 (2014).
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 Yu F, Zheng J, Mao Y, Dong P, Li G, Lu Z, et al. Long non-coding RNA APTR promotes the activation of hepatic stellate cells and the progression of liver fibrosis[J]. Biochemical and biophysical research communications.2015,463(4):679-85.
Basic Information
Transcript ID |
NONHSAT121673 |
Source |
NONCODE4.0 |
Same with |
APTR ,RSBN1L-AS1 |
Classification |
intergenic |
Length |
1978 nt |
Genomic location |
chr7-:77311382..77325742 |
Exon number |
3 |
Exons |
77311382..77313568,77314519..77314645,77325213..77325742 |
Genome context |
|
Sequence |
000001 GGAGAGTCCT CAAGATGGAT TTTCACAAAT CCTGCAGCGC ACTAACTGGG AGGAAGAAAC GATACAGAAA ATAAGAGTGT 000080
000081 CGGCCATCCC CCTCTCTGCA ACCGAAATTA CAGGCTCCAT TTCCTGTCCC CTTGGGAACT GCAAAATCCT CTGCTGAAAA 000160 000161 CCGGACGCCT CCCAGCCCCT CCAGGCCGGC GCACGCGGCC GCCGCGCTCC CCCTTCCCGG GCCCCGTGGG CGCCAGGGGG 000240 000241 CGGCGGGGAC CCACGGCGCC CTCCCCTCCC CCTCCCCGCA CGGCACCCAC CTCGGGGCAG CGGCTTCACC TCCCCGTTCT 000320 000321 CCTCCCGGGA GGCCCCGCCG GCCTCTCGGG CCCCACCGAG ACCGTGCCTC CTCCTCTCCT TCTCCCGCTT CTCCTTAGGT 000400 000401 CTGCGCGACT TGGCGTTAGC CGAGGCAGCG GCGGCGGCGG CGGGCAGGAG GAGATGGTGA GGCTGAGCGT GCAGCAGCGT 000480 000481 AGGAGGGACC AGCAGTTTGC GCGGCACCGG CTGAGACAAG GAAGCGGAGG CTGAGGAGGG AACGGCCGTG CCAGCGGAGA 000560 000561 AAGAGAAACT GCTCCGAGAA GAGGACGGGG AGGGAGCAGC AGACAGAGGG GCAAAGCTCC AAGACGCGGG GCTGCCATAG 000640 000641 CTCTGAGGCG AAGGTGCTGC CGGCGGCTGC AGCTGCCTGC TGTTCCCGCC GCTGCCCCCT TCTCCGTTCA CTCTCCGCGG 000720 000721 TGCCTTCTTC TCCTCAGTCC GGACCTTCTT GGCGGACAGA GAACCCGGAG GGTCCCGGGA GGAGAGTTGC AGCTTGCCAA 000800 000801 ACGGTTCTTT CTCCGAGACG GTGGCGGTGG GGGCCGCGGC AGCGACACAG TGCACGGGGC TCGGCGGTTC CGCCATTTTG 000880 000881 CGCTCCTGTT GTATTTACTC TCCTCCGCTA GCCGGCGCGG GGCAGGGGGC GGGCCCTCCG CGAGGGGTAG GGAAGGGGCG 000960 000961 GAGCGGCCAG GCCACCAGCC GGCATTGCTC CATTGGGCAA GCCACGCTGA GGGATCCACC TAAGAGCCAA TCAAAGGCAC 001040 001041 AAACATCAGA CGAAGGGGCG GGATCGCCAC AGGGACCCTC TTCGGAGGTC AGAGCTCGGC GGGGTGCGGC TAGTGGCGGA 001120 001121 GCGCGCTGCG AGGGGAGGGC TTTCCACTGT CGCTGGCGTG AACTCGCGTG CCCGGTGGGT ATCAGGGAAG AACCCCCGCC 001200 001201 CCGGACCCCC AGATCTGCCA TGGCCGAGGT AGCGATCGTC TCTGCGGCCA CGAAGACTGT TTTAACTTGT ACCACTTTCC 001280 001281 CTTCCATTTT TCCTGGGGTG CCTCTCACCC TGCATCTGCG CGTTCAGCAA GCTGGATTTC GGGAATGCTC AGTTCAGAAG 001360 001361 AGAAAAAATT GCCGGGAATC AAGTCCTTCT TTTTGTTAGT CGGTAGTCGA TTGATGGGAA GTGTTCAAAA TCATTCGATG 001440 001441 TGGTGACAAG GCTTCACCAG GTACTGCCTT CTAACGAGCT GGCCATTTCC ACATGTCAGA TAGGACCAAC TTGCCTTTTA 001520 001521 ACTACCCGTG TGATACTTAA ACACTGTTGC CGGTATCACA GCTTTTCTTC AAAACAGGAA GCAACGAGAA TGAGGGCATT 001600 001601 CCAGTAGCAG GAGACAGCAT GCATAGAGAT GCTGATGAAG AAAGAGCCTA GCGCACGTGG GAAACTGCAA AAGTTCAGAC 001680 001681 TGGTTGGAAT GCTGGAAATG TTGTGAATGA CAGGAGATGA GGCTGGCGAG AAAACAGAGG TCAGATTGTG GAAGGCTGTC 001760 001761 AAGCCAAAGA CTTTGATTTT ATTCTTGAGA TTGATGAGAT GTGTGTAATC CAGGAGTGTG CAAAACAATC TGTAAGGGTT 001840 001841 CAGAAAACAT ACTGCTTCTA TATATAGTTA CCTTTGTCTT AACTTGAAAA TTTCAAATTG TGTAGGAGTT ACAATGTGTG 001920 001921 TAATTGTTAT TATAGTACTG GATCCAAATA ATTTATAAAT AAATAAATAT AGACATAA |