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PKCδ stabilizes TAp63 to promote cell apoptosis
Author(s) -
Li Decai,
Li Chenghua,
Wu Min,
Chen Qiongqiong,
Wang Qiao,
Ren Jian,
Zhang Yujun
Publication year - 2015
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2015.06.014
Subject(s) - apoptosis , microbiology and biotechnology , chemistry , protein kinase c , biophysics , signal transduction , biology , biochemistry
PKCδ and p63 are respectively reported to play important roles in cell apoptosis. But there is no report on interaction between them in regulation of apoptosis. In the present study, we found that PKCδ can directly associate and up‐regulate TA isoforms of p63 (TAp63) proteins via increasing their stability. PKCδ kinase activity and Thr157 site in TAp63 are crucial for this PKCδ‐induced accumulation of TAp63. PKCδ can also enhance TAp63‐mediated transcription and cell apoptosis. Taken together, our data indicate that PKCδ phosphorylates TAp63 proteins at Thr157 to stabilize them and promote cell apoptosis.

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