期刊
FEBS LETTERS
卷 589, 期 23, 页码 3686-3690出版社
WILEY
DOI: 10.1016/j.febslet.2015.10.028
关键词
c-Jun N-terminal kinase 1; TAp63 gamma; Transactivity; Apoptosis
资金
- National Natural Science Foundation of China [31100982]
- Research Foundation for the Doctoral Program, Ministry of Education of China [20110181120082]
TAp63 gamma is a homologue of tumor suppressor p53 and functions as a transcriptional factor playing key roles in cell cycle and cell apoptosis. In the present work, we find that JNK1 can physically interact with N-terminal transactivation domain (TAD) of TAp63. Overexpression of JNK1 inhibits TAp63 gamma-mediated transcription, while knockdown or inhibition of endogenous JNK1 increases transactivity of TAp63 gamma. Further study reveals that Ser12 site in TAD is critical for JNK1-mediated inhibition of TAp63 gamma. This JNK1-mediated inhibition can impair pro-apoptotic activity of TAp63 gamma. Together, we report a novel regulation of TAp63 gamma transactivity and pro-apoptotic activity mediated by JNK1. (C) 2015 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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