Difference between revisions of "ABALON"
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INXS lncRNA induces tumor regression in vivo when it is overexpressed <ref name="ref1" />. | INXS lncRNA induces tumor regression in vivo when it is overexpressed <ref name="ref1" />. | ||
| + | ===Regulation=== | ||
| + | INXS expression is driven by a directional promoter, which contain a GC box and TATA box upstream of the INXS transcription start site. When treated with apoptosis-inducing agents, with increased BCL-XS mRNA, the expression of INXS will also increase. <ref name="ref1" /> | ||
| + | ===Diseases=== | ||
| + | * tumor suppressor <ref name="ref1" /> | ||
| + | |||
| + | ===Expression=== | ||
| + | INXS expression level in tumor cell lines from kidney, liver, breast and prostate is 5- to 9-fold lower compared with non-tumor cell lines derived from the same tissues. In patients with renal cell carcinoma, INXS levels are 2- to 60-fold lower in the tumor tissue compared with the matched non-tumor.<ref name="ref1" /> | ||
{| class='wikitable' style="text-align:center" | {| class='wikitable' style="text-align:center" | ||
Revision as of 11:06, 30 June 2017
ABALON, which is transcribed from the opposite genomic strand of BCL-X and lowly expressed in many tumors, functions to induce BCL-XS isoform and cause apoptosis, exhibiting tumor suppressor activity.
Contents
Annotated Information
Name
ABALON: apoptotic BCL2L1-antisense long non-coding RNA (HGNC nomenclature)
INXS: intronic BCL-XS-inducing lncRNA [1]
Characteristics
INXS is an unspliced 1903 nt-long RNA, transcribed by RNA polymerase Ⅱ, 5’-capped. The full length transcript spanned beyond exons 1 and 2, overlapping intron 1 and some of the genomic regions upstream of BCL-X. The half-life of INXS was determined to be ∼3 h, indicating it is stable. [1]
It belongs to the category of "Antisense" in lncRNA classification.
Cellular Localization
INXS is a nuclear-enriched transcript [1].
Function
INXS functions as a critical mediator of BCL-XS splice regulation. Overexpression of INXS will induce BCL-XS isoform accumulation and lead to apoptosis in vitro by activating caspases 3, 7 and 9. INXS may interact with Sam68 splicing-modulator complex to regulate the alternative splicing of BCL-X pre-mRNA, but overexpression or knockdown of INXS does not affect the splicing of other Sam68 target mRNAs [1].
INXS lncRNA induces tumor regression in vivo when it is overexpressed [1].
Regulation
INXS expression is driven by a directional promoter, which contain a GC box and TATA box upstream of the INXS transcription start site. When treated with apoptosis-inducing agents, with increased BCL-XS mRNA, the expression of INXS will also increase. [1]
Diseases
- tumor suppressor [1]
Expression
INXS expression level in tumor cell lines from kidney, liver, breast and prostate is 5- to 9-fold lower compared with non-tumor cell lines derived from the same tissues. In patients with renal cell carcinoma, INXS levels are 2- to 60-fold lower in the tumor tissue compared with the matched non-tumor.[1]
| Primer | Forward primer | Reverse primer |
|---|---|---|
| RT-PCR | 5'-CCCCCTCCAGGTACCAGAAC-3' | 5'-CCACTGGTGCTTTCGATTTGA-3'[1] |
| Cloning | 5'-AGTAGCTAGCGTGGTGAAATGAGGCCAGTC-3' | 5'-TTATCTCGAGCAGGAAAACGTGGTCTCAGC-3'[1] |
| Knockdown | INXS ASO-1 | 5'-mG*mC*mC*mU*mC*A*C*C*C*T*C*A*C*C*C*mA*mG*mU*mC*mU-3'[1] |
| INXS ASO-2 | 5'-mC*mA*mC*mC*mU*C*C*T*C*T*C*C*C*G*A*mC*mC*mU*mG*mU-3'[1] |
Sequence
>gi|558605735|gb|KC505631.1| Homo sapiens INXS lncRNA, complete sequence
000081 AGAAGGGCTG TTGGGGATCT CTGACCAGAG GCCAAAGAAA AGGGACACAC AAGGGGCTTG GTTCTTACCC AGCCGCCGTT 000160
000161 CTCCTGGATC CAAGGCTCTA GGTGGTCATT CAGGTAAGTG GCCATCCAAG CTGCGATCCG ACTCACCAAT ACCTGCATCT 000240
000241 CCTTGTCTAC GCTTTCCACG CACAGTGCCC CGCCGAAGGA GAAAAAGGCC ACAATGCGAC CCCAGTTTAC CCCATCCCGG 000320
000321 AAGAGTTCAT TCACTACCTG TTCAAAGCTC TGATATGCTG TCCCTGGGGT GATGTGGAGC TGGGATGTCA GGTCACTGAA 000400
000401 TGCCCGCCGG TACCGCAGTT CAAACTCGTC GCCTGCCTCC CTCAGCGCTT GCTTTACTGC TGCCATGGGG ATCACCTCCC 000480
000481 GGGCATCCAA ACTGCTGCTG TGGCCAGTGG CTCCATTCAC CGCGGGGCTG TCTGCCAGGT GCCAGGATGG GTTGCCATTG 000560
000561 ATGGCACTGG GGGTCTCCAT CTCCGATTCA GTCCCTTCTG GGGCCTCAGT CCTGTTCTCT TCCACATCAC TAAACTGACT 000640
000641 CCAGCTGTAT CCTTTCTGGG AAAGCTTGTA GGAGAGAAAG TCAACCACCA GCTCCCGGTT GCTCTGAGAC ATTTTTATAA 000720
000721 TAGGGATGGG CTCAACCAGT CCATTGTCCA AAACACCTGC TCACTCACTG AGTCTCGTCT CTGGTTAGTG ATTCTCTTCT 000800
000801 AAGATCCAAA GCCAAGATAA GATTCTGAAG GGAGAGAAAG AGCTTCAGGA AAAAAAAATA ATTAATATGC ATGCCATTTA 000880
000881 CCCTAAAAAT TCCATTCCCC CTCCAGGTAC CAGAACTGGT TTCTTTGTGG GTCTTACGAA GGTCTGGGTC TAGGTTCCAA 000960
000961 GATACTTCAC TTAAGTCAAA TCGAAAGCAC CAGTGGACTC TGAATCTCCC ACCAGCCTTT TCTACCCCCG TCTTCTCCGA 001040
001041 AATGCCTTCC TCGGAAAGTC ACTCCCTGGG CAGTCCCCCC CGCCCCACTC CCGCTCCCCC GCACCACCTA CATTCAAATC 001120
001121 CGCCTTAGGC AAAGGCAGGC AGGTGCAGCC CCCGGAAGAT CTTTTGTATC ACAGGTCGGG AGAGGAGGTG GCTGCGGGGA 001200
001201 TGCCGGTAAC TCAGCCGGCC TCGCGGTGGC TGGCAAAAAA ACCAGCTCCG GCCGGAGGGA TCATGCGACC CGGCAGGCTG 001280
001281 GGAGCCCAGA AGGCGACACA GGAATTGCGA AGCTCAGGAA CCAGCCCCCT CGCTTGCTTC CTCCTCCATC GCCCGGATCG 001360
001361 AGGGCGGCCG CTCCGCAGCC GCGGCCTCCT GCCACCCGGG AGCCCAGCCC CCTCTCTCTT GCACGCCCCT TGGCTCTCCG 001440
001441 CCTCCTACTG GGAGCCAGGA GTACTCTCCC GGAGGTGGCT GGTATGGATT TAGTTGGTTT TTGTTTTTCT TTTTTCTATT 001520
001521 TAAGCACCAG CCCAGGGTGA GGTGGAGGCG TCCGAAACCC TAAAGGGACT TCTCAATGGG GTTCAAGGTT TCAGTGAGGG 001600
001601 ACGCAGGGAG GGGGAAACTG CCTCAGATCT GCAATCTGAC TTTGGGAAGG CCACCCCCAG GCCTGTCTGT GATGTTGAAG 001680
001681 GCCGGAGACC CCCAACAAAT GCCGCTGGTT TGCTCTGAAT TCCCCAAAGG CCCAGAACGT GGCAGTTGGG GATTGCCGGG 001760
001761 TCCTCCATTC CCCGCCCGGA CACAATGGCC GCCGGCGCCC TGCACAAAGA CTGGGTGAGG GTGAGGCGCT GGGCCTCTCC 001840
001841 TCAGGTCAGG AAGAGGGGTC GAGGCCTGCT CGACGGCCCC ACAGCTGAGA CCACGTTTTC CTG
Labs working on this lncRNA
- Departamento de Bioqu´ımica, Instituto de Qu´ımica, Universidade de S˜ao Paulo, 05508-900 S˜ao Paulo, SP, Brasil [1].
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 DeOcesano-Pereira, C., Amaral, M.S., Parreira, K.S., Ayupe, A.C., Jacysyn, J.F., Amarante-Mendes, G.P., Reis, E.M. and Verjovski-Almeida, S. (2014) Long non-coding RNA INXS is a critical mediator of BCL-XS induced apoptosis. Nucleic Acids Res, 42, 8343-8355.
