期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 355, 期 1, 页码 263-268出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2007.01.146
关键词
p21(WAF1/CIP1); JNK; H2O2; proteasome; ubiquitination; stabilization
Proteasome-dependent degradation of regulatory proteins is a known mechanism of cell cycle control. p21(WAF1/CIP1)(p21), a negative regulator of the cell division cycle, exhibits proteasome-sensitive turnover and ubiquitination. In the present study, we analyzed the regulatory effects of JNKI on p21 protein accumulation in p53 null K562 cells. We found that JNK1 (wild type, WT) mediated H2O2-induced p21 protein up-regulation. Over-expression of JNKI (WT) could elevate endogenous p21 protein level but did not affect p21 mRNA level and also prolong the p21 half-life as well as inhibited the p21 ubiquitination. These findings indicated that JNKI could regulate cellular p21 level via inhibiting ubiquitination of p21, which provided a new insight for analyzing the regulatory effect of JNK after stress. (c) 2007 Elsevier Inc. All rights reserved.
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