STAT1
车站3
糖蛋白130
STAT蛋白
癌基因
转录因子
生物
癌症研究
发起人
基因
信号转导
细胞生物学
基因表达
遗传学
细胞周期
作者
Davide Schiavone,Lidia Avalle,Sarah Dewilde,Valeria Poli
出处
期刊:FEBS Letters
[Wiley]
日期:2011-06-28
卷期号:585 (15): 2455-2460
被引量:36
标识
DOI:10.1016/j.febslet.2011.06.020
摘要
Signal transducer and activators of transcription (STAT)1 and STAT3 cross‐regulate their activity downstream of gp130 cytokines, and eliminating STAT3 leads to IFN‐γ‐like responses to IL‐6 correlating with prolonged STAT1 phosphorylation. Here we demonstrate that the increased gp130‐mediated induction of the IFN‐γ‐responsive interferon regulatory factor 1 gene observed in STAT3 −/− cells correlates with prolonged STAT1 binding to its promoter. Intriguingly, gp130‐mediated induction of the immediate early genes FBJ osteosarcoma oncogene and early growth response 1 is also prolonged in STAT3 −/− cells, with STAT1 binding to their promoters. Thus the abrogation of STAT3 expression, perturbing the signaling balance, directs the STAT1 oncosuppressor to transcribe new target genes, known to drive mitogen responses and tumor transformation.
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