DJ-1 decreases Bax expression through repressing p53 transcriptional activity
DJ-1 decreases Bax expression through repressing p53 transcriptional activity
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DJ-1 通过抑制 p53 转录活性降低 Bax 表达
DOI：
10.1074/jbc.m707176200
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发表时间：
2008-02-15
影响因子：
4.8
通讯作者：
Wang, Guanghui
中科院分区：
文献类型：
--
作者：
Fan, Jun;Ren, Haigang;Wang, Guanghui
DJ-1最初被鉴定为癌基因产物，是一种在细胞转化、氧化应激反应和转录调节中具有多种功能的蛋白质。虽然以前的研究表明DJ-1是细胞保护，DJ-1发挥其生存功能的机制仍然在很大程度上未知。我们发现DJ-1通过抑制p53-p53-caspase通路发挥其细胞保护作用。DJ-1与p53在体外和体内相互作用。DJ-1的过表达降低Bax的表达并抑制caspase的活化，而DJ-1的敲低增加Bax蛋白水平并加速caspase-3的活化和UV暴露诱导的细胞死亡.我们的数据提供了证据表明，DJ-1对细胞凋亡的保护作用与其通过抑制p53转录活性降低Bax水平的能力有关。
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.