HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

J. Biol. Chem., Vol. 283, Issue 7, 4022-4030, February 15, 2008

This Article Full Text Full Text (PDF) All Versions of this Article: 283/7/4022    most recent M707176200v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Fan, J. Articles by Wang, G. PubMed PubMed Citation Articles by Fan, J. Articles by Wang, G. Social Bookmarking                      What's this?

DJ-1 Decreases Bax Expression through Repressing p53 Transcriptional Activity^*

From the Laboratory of Molecular Neuropathology, Hefei National Laboratory for Physical Sciences at Microscale and School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China

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 knockdown 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.

Received for publication, August 27, 2007 , and in revised form, November 26, 2007.

^* This work was supported in part by National Natural Sciences Foundation of China Grant 30770664, National High-tech Research and Development program of China 973-project 2006CB500703 and 863-project 2006AA02Z184, and the Chinese Academy of Sciences Knowledge Innovation Project (KSCX2-YW-R-138). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed. Tel. and Fax: 86-551-3607058; E-mail: wghui{at}ustc.edu.cn.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?