Difference between revisions of "BGLT3"

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(Function)
(Synonyms)
 
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===Synonyms===
 
===Synonyms===
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[[File:Altering lncRNA-BGL3 expression significantly affects tumor formation induced by K562 leukemic cells in xenograft mouse model.png|right|thumb|500px|'''Altering lncRNA-BGL3 expression significantly affects tumor formation induced by K562 leukemic cells in xenograft mouse model.''' <ref name="ref1" />.]]
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LINC01083, BGL3, lncRNA-BGL3
 
LINC01083, BGL3, lncRNA-BGL3
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===Chromosome===
 
===Chromosome===
 
11p15.4
 
11p15.4
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ENSG00000260629
 
ENSG00000260629
 
===Function===
 
===Function===
[[File:Altering lncRNA-BGL3 expression significantly affects tumor formation induced by K562 leukemic cells in xenograft mouse model|right|thumb|200px|'''Altering lncRNA-BGL3 expression significantly affects tumor formation induced by K562 leukemic cells in xenograft mouse model.''' <ref name="ref1" />.]]
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lncRNA-BGL3 that acted as a key regulator of Bcr-Abl-mediated cellular transformation.<ref name="ref1" />
 
lncRNA-BGL3 that acted as a key regulator of Bcr-Abl-mediated cellular transformation.<ref name="ref1" />

Latest revision as of 07:40, 28 June 2016

Annotated Information

Approved Symbol

BGLT3:beta globin locus transcript 3 (non-protein coding)

Synonyms

Altering lncRNA-BGL3 expression significantly affects tumor formation induced by K562 leukemic cells in xenograft mouse model. [1].

LINC01083, BGL3, lncRNA-BGL3

Chromosome

11p15.4

RefSeq ID

NR_121648

OMIM ID

616308

Ensembl ID

ENSG00000260629

Function

lncRNA-BGL3 that acted as a key regulator of Bcr-Abl-mediated cellular transformation.[1]

TG expression of lncRNA-BGL3 alone in mice was sufficient to impair primary bone marrow transformation by Bcr-Abl.[1]

lncRNA-BGL3 was a target of miR-17, miR-93, miR-20a, miR-20b, miR-106a and miR-106b, microRNAs that repress mRNA of phosphatase and tensin homolog (PTEN). [1]

Expression

lncRNA-BGL3 was highly induced in response to disruption of Bcr-Abl expression or by inhibiting Bcr-Abl kinase activity in K562 cells and leukemic cells derived from CML patients. [1]

Ectopic expression of lncRNA-BGL3 sensitized leukemic cells to undergo apoptosis and inhibited Bcr-Abl-induced tumorigenesis. [1]

Disease

  • Bcr-Abl-positive leukemia [1]

Labs working on this lncRNA

  • CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, China.[1]

References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 Guo G, Kang Q, Zhu X, Chen Q, Wang X, Chen Y, et al. A long noncoding RNA critically regulates Bcr-Abl-mediated cellular transformation by acting as a competitive endogenous RNA[J]. Oncogene. 2015,34(14):1768-79.

Sequence

>gi|656985089|ref|NR_121648.1| Homo sapiens beta globin locus transcript 3 (non-protein coding) (BGLT3), long non-coding RNA

000001 TTAGCAGTAA CTGCTGAATT CCTGGTTGGC TGATGGAAAG ATGGGGCAGC TGTTCACTGG TACGCAGGGT TTTAGATGTA 000080
000081 TGTACCTAAG GATATGAGGT ATGGCAATGA ACAGAAATTC TTTTGGGAAT GAGTTTTAGG GCCATTAAAG GACATGACCT 000160
000161 GAAGTTTCCT CTGAGGCCAG TCCCCACAAC TCAATATAAA TGTGTTTCCT GCATATAGTC AAAGTTGCCA CTTCTTTTTC 000240
000241 TTCATATCAT CGATCTCTGC TCTTAAAGAT AATCTTGGTT TTGCCTCAAA CTGTTTGTCA CTACAAACTT TCCCCATGTT 000320
000321 CCTAAGTAAA ACAGGTAACT GCCTCTCAAC TATATCAAGT AGACTAAAAT ATTGTGTCTC TAATATCAGA AATTCAGCTT 000400
000401 TAATATATTG GGTTTAACTC TTTGAAATTT AGAGTCTCCT TGAAATACAC ATGGGGGTGA TTTCCTAAAC TTTATTTCTT 000480
000481 GTAAGGATTT ATCTCAGGGG TAACACACAA ACCAGCATCC TGAACCTCTA AGTATGAGGA CAGTAAGCCT TAAGAATATA 000560
000561 AAATAAACTG TTCTTCTCTC TGCCGGTGGA AGTGTGCCCT GTCTATTCCT GAAATTGCTT GTTTGAGACG CATGAGACGT 000640
000641 GCAGCACATG AGACACGTGC AGCAGCCTGT GGAATATTGT CAGTGAAGAA TGTCTTTGCC TGATTAGATA TAAAGACAAG 000720
000721 TTAAACACAG CATTAGACTA TAGATCAAGC CTGTGCCAGA CACAAATGAC CTAATGCCCA GCACGGGCCA CGGAATCTCC 000800
000801 TATCCTCTTG CTTGAACAGA GCAGCACACT TCTCCCCCAA CACTATTAGA TGTTCTGGCA TAATTTTGTA GATATGTAGG 000880
000881 ATTTGACATG GACTATTGTT CAATGATTCA GAGGAAATCT CCTTTGTTCA GATAAGTACA CTGACTACTA AATGGATTAA 000960
000961 AAAACACAGT AATAAAACCC AGTTTTCCCC TTAAAAAAAA AAAAAAAAAA AAAAAAAAA