Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 278, Issue 3, Pages 2066-2071Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M206697200
Keywords
-
Categories
Funding
- NCI NIH HHS [CA88406] Funding Source: Medline
Ask authors/readers for more resources
The p53 tumor suppressor is stabilized and activated by diverse stress signals. In this study, we investigated the mechanism of p53 activation by heat shock. We found that heat shock inhibited p53 ubiquitination and caused accumulation of p53 at the post-transcriptional level. Heat shock induced phosphorylation of p53 at serine 15 in an ATM kinase-dependent fashion, which may contribute partially to heat-induced p53 accumulation. However, p53 accumulation also occurred after heat shock in ATM-deficient cells. Heat shock induced conformational change of wild type p53 and binding to hsp90. Inhibition of hsp90-p53 interaction by geldanamycin prevented p53 accumulation partially in ATM-wild type cells and completely in ATM-deficient cells. Therefore, phosphorylation and interaction with hsp90 both contribute to stabilization of p53 after heat shock.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available