The prosurvival Bcl-2 homolog Bfl-1/A1 is a direct transcriptional target of NF-κB that blocks TNFα-induced apoptosis

被引:624
作者
Zong, WX
Edelstein, LC
Chen, CL
Bash, J
Gélinas, C [1 ]
机构
[1] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Ctr Adv Biotechnol & Med, Piscataway, NJ 08854 USA
[2] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Grad Program Biochem & Mol Biol, Piscataway, NJ 08854 USA
[3] Rutgers State Univ, Grad Program Microbiol & Mol Genet, Piscataway, NJ 08854 USA
[4] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Biochem, Piscataway, NJ 08854 USA
关键词
Rel; NF-kappa B; Bfl-1; A1; TNF alpha; apoptosis;
D O I
10.1101/gad.13.4.382
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
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-kappa B. We show that bfl-1 gene expression is dependent on NF-kappa B activity and that it can substitute for NF-kappa B to suppress TNF alpha-induced apoptosis. bfl-1 promoter analysis identified an NE-KB site responsible for its Rel/NF-kappa B-dependent induction. The expression of bfl-1 in immune tissues supports the protective role of NF-kappa B in the immune system. The activation of Bfl-1 may be the means by which NF-KB functions in oncogenesis and promotes cell resistance to anti-cancer therapy.
引用
收藏
页码:382 / 387
页数:6
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