PKCδ stabilizes TAp63 to promote cell apoptosis
PKCδ stabilizes TAp63 to promote cell apoptosis
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PKCδ 稳定 TAp63 以促进细胞凋亡
DOI：
10.1016/j.febslet.2015.06.014
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发表时间：
2015-07-22
期刊：
影响因子：
3.5
通讯作者：
Zhang, Yujun
中科院分区：
文献类型：
--
作者：
Li, Decai;Li, Chenghua;Zhang, Yujun
据报道，PKC δ 和 p63 分别在细胞凋亡中发挥重要作用。但二者在细胞凋亡调控中的相互作用尚未见报道。在本研究中，我们发现 PKC delta 可以通过增加 p63 (TAp63) 蛋白的 TA 亚型的稳定性来直接关联和上调它们。 PKC δ 激酶活性和 TAp63 中的 Thr157 位点对于 PKC δ 诱导的 TAp63 积累至关重要。 PKC delta 还可以增强 TAp63 介导的转录和细胞凋亡。综上所述，我们的数据表明 PKCS 在 Thr157 处磷酸化 TAp63 蛋白以稳定它们并促进细胞凋亡。 (C) 2015 年欧洲生化学会联合会。由 Elsevier B.V. 出版。保留所有权利。
PKC delta 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 PKC delta can directly associate and up-regulate TA isoforms of p63 (TAp63) proteins via increasing their stability. PKC delta kinase activity and Thr157 site in TAp63 are crucial for this PKC delta-induced accumulation of TAp63. PKC delta can also enhance TAp63-mediated transcription and cell apoptosis. Taken together, our data indicate that PKCS phosphorylates TAp63 proteins at Thr157 to stabilize them and promote cell apoptosis. (C) 2015 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.