Arginine methylation of hnRNP K enhances p53 transcriptional activity

被引:40
作者
Chen, Yibin [1 ]
Zhou, Xinyuan [1 ]
Liu, Na [2 ,3 ]
Wang, Chaochen [1 ]
Zhang, Liang [1 ]
Mo, Wei [1 ]
Hu, Gengxi [1 ]
机构
[1] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, State Key Lab Mol Biol, Shanghai 200031, Peoples R China
[2] Univ Sci & Technol China, Hefei Natl Lab Phys Sci Microscale, Hefei, Anhui, Peoples R China
[3] Univ Sci & Technol China, Dept Neurobiol, Sch Life Sci, Hefei, Anhui, Peoples R China
来源
FEBS LETTERS | 2008年 / 582卷 / 12期
关键词
hnRNP K; UV radiation; arginine methylation; p53; transcriptional regulation;
D O I
10.1016/j.febslet.2008.04.051
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
Previous studies have illustrated that hnRNP K, which could be methylated at arginine residues, plays a key role in coordinating transcriptional responses to DNA damage as a cofactor for p53. In this study, we observed that hnRNP K was markedly arginine methylated in response to UV radiation. Furthermore, arginine methylation of hnRNP K enhanced its affinity with p53. Inhibition of methylation in hnRNP K attenuated the recruitment of p53 to p21 promoter, and reduced p53 transcriptional activity. These data suggested that arginine methylation of hnRNP K is a key element for p53 transcriptional activity. (C) 2008 Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.
引用
收藏
页码:1761 / 1765
页数:5
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