DJ-1 decreases Bax expression through repressing p53 transcriptional activity.
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.
Mesh Terms:
Apoptosis, Base Sequence, Caspases, Cell Line, DNA Primers, Humans, Hydrogen Peroxide, Immunoprecipitation, Intracellular Signaling Peptides and Proteins, Oncogene Proteins, Transcription, Genetic, Tumor Suppressor Protein p53, Ultraviolet Rays, bcl-2-Associated X Protein
Apoptosis, Base Sequence, Caspases, Cell Line, DNA Primers, Humans, Hydrogen Peroxide, Immunoprecipitation, Intracellular Signaling Peptides and Proteins, Oncogene Proteins, Transcription, Genetic, Tumor Suppressor Protein p53, Ultraviolet Rays, bcl-2-Associated X Protein
J. Biol. Chem.
Date: Feb. 15, 2008
PubMed ID: 18042550
View in: Pubmed Google Scholar
Download Curated Data For This Publication
147824
Switch View:
- Interactions 2