DJ-1 decreases Bax expression through repressing p53 transcriptional activity

被引：201

作者：

Fan, Jun ^{[1
]}

Ren, Haigang ^{[1
]}

Jia, Nali ^{[1
]}

Fei, Erkang ^{[1
]}

Zhou, Tian ^{[1
]}

Jiang, Peng ^{[1
]}

Wu, Mian ^{[1
]}

Wang, Guanghui ^{[1
]}

机构：

[1] Univ Sci & Technol China, Lab Mol Neuropathol, Hefei Natl Lab Phys Sci Microscale, Sch Life Sci, Hefei 230027, Anhui, Peoples R China

来源：

JOURNAL OF BIOLOGICAL CHEMISTRY | 2008年 / 283卷 / 07期

关键词：

D O I：

10.1074/jbc.M707176200

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

DJ-1, originally identified as an oncogene product, is a protein with various functions in cellular transformation, oxidative stress response, and transcriptional regulation. Although previous studies suggest that DJ-1 is cytoprotective, the mechanism by which DJ-1 exerts its survival functions remains largely unknown. Here we show that DJ-1 exerts its cytoprotection through inhibiting p53-Bax-caspase pathway. DJ-1 interacts with p53 in vitro and in vivo. Overexpression of DJ-1 decreases the expression of Bax and inhibits caspase activation, whereas knock- down of DJ-1 increases Bax protein levels and accelerates caspase-3 activation and cell death induced by UV exposure. Our data provide evidence that the protective effects of DJ-1 on apoptosis are associated with its ability of decreasing Bax level through inhibiting p53 transcriptional activity.

引用

页码：4022 / 4030

页数：9

共 56 条

[21] Histone deacetylases specifically down-regulate p53-dependent gene activation [J].