生物
NF-κB
细胞凋亡
NFKB1型
癌变
肿瘤坏死因子α
细胞生物学
癌症研究
免疫系统
基因
转录因子
遗传学
免疫学
作者
W-X Zong,Leonard C. Edelstein,Chi Chen,J. Bash,Céline Gélinas
出处
期刊:Genes & Development
[Cold Spring Harbor Laboratory Press]
日期:1999-02-15
卷期号:13 (4): 382-387
被引量:720
摘要
Bcl-2-family proteins are key regulators of the apoptotic response. Here, we demonstrate that the pro-survival Bcl-2 homolog Bfl-1/A1 is a direct transcriptional target of NF-kappaB. We show that bfl-1 gene expression is dependent on NF-kappaB activity and that it can substitute for NF-kappaB to suppress TNFalpha-induced apoptosis. bfl-1 promoter analysis identified an NF-kappaB site responsible for its Rel/NF-kappaB-dependent induction. The expression of bfl-1 in immune tissues supports the protective role of NF-kappaB in the immune system. The activation of Bfl-1 may be the means by which NF-kappaB functions in oncogenesis and promotes cell resistance to anti-cancer therapy.
科研通智能强力驱动
Strongly Powered by AbleSci AI