JNK1 inhibits transcriptional and pro-apoptotic activity of TAp63γ.

TAp63γ 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 TAp63γ-mediated transcription, while knockdown or inhibition of endogenous JNK1 increases transactivity of TAp63γ. Further study reveals that Ser12 site in TAD is critical for JNK1-mediated inhibition of TAp63γ. This JNK1-mediated inhibition can impair pro-apoptotic activity of TAp63γ. Together, we report a novel regulation of TAp63γ transactivity and pro-apoptotic activity mediated by JNK1. [ABSTRACT FROM AUTHOR]