c-Jun NH2-terminal kinase decreases ubiquitination and promotes stabilization of p21WAF1/CIP1 in K562 cell

被引：16

作者：

Fan, Yumei

Chen, Hui

Qiao, Bo

Liu, Ziwen

Luo, Lan

Wu, Yifan

Yin, Zhimin ^{[1
]}

机构：

[1] Nanjing Normal Univ, Jiangsu Prov Key Lab Mol & Med Biotechnol, Coll Life Sci, Nanjing 210097, Peoples R China

[2] Nanjing Univ, State Key Lab Pharmaceut Biotechnol, Sch Life Sci, Nanjing 210093, Peoples R China

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2007年 / 355卷 / 01期

关键词：

p21(WAF1/CIP1); JNK; H2O2; proteasome; ubiquitination; stabilization;

D O I：

10.1016/j.bbrc.2007.01.146

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：263 / 268

页数：6

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