4.5 Article

JNK1 inhibits transcriptional and pro-apoptotic activity of TAp63γ

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

  1. National Natural Science Foundation of China [31100982]
  2. Research Foundation for the Doctoral Program, Ministry of Education of China [20110181120082]

向作者/读者索取更多资源

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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