Opposing Effects of Protein Kinase C δ and Protein Kinase B α on H2O2-Induced Apoptosis in CHO Cells☆
Opposing Effects of Protein Kinase C δ and Protein Kinase B α on H2O2-Induced Apoptosis in CHO Cells☆
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蛋白激酶Cδ和蛋白激酶Bα对H2O2诱导的CHO细胞凋亡的相反作用☆
DOI：
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发表时间：
1999
期刊：
影响因子：
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通讯作者：
U. Kikkawa
中科院分区：
文献类型：
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作者：
H. Konishi;H. Matsuzaki;H. Takaishi;Toshiyoshi Yamamoto;M. Fukunaga;Y. Ono;U. Kikkawa
摘要DNA片段分析表明，过氧化氢诱导的蛋白激酶C δ（PKCδ）高表达的CHO细胞凋亡增强。H2O2处理后，PKCδ被酪氨酸磷酸化并恢复为组成型活性形式，但不产生蛋白水解片段。相反，过表达蛋白激酶B α（PK B α）的CHO细胞系中H2O2诱导的凋亡受到抑制。结论：PKBα对BAD的磷酸化有负调控作用，而PKCδ对BAD的磷酸化无影响。在同时过表达PKCδ和PKBα的CHO细胞系中，H2O2诱导的PKCδ酪氨酸磷酸化被抑制，DNA断裂也随之减少。这些结果表明，PKCδ通过独立于BAD的机制参与H2O2诱导的细胞凋亡，并且PKCδ是PKB调节细胞存活的靶点。
Abstract H2O2-induced apoptosis was enhanced in the CHO cell line overproducing protein kinase C δ (PKCδ) as judged by DNA fragmentation. In response to the H2O2 treatment, PKCδ was tyrosine phosphorylated and recovered as a constitutively active form, but its proteolytic fragment was not generated. In contrast, H2O2-induced apoptosis was suppressed in the CHO cell line overexpressing protein kinase B α (PKBα). Consistently, phosphorylation of BAD, a pro-apoptotic protein negatively regulated by PKBα, was sustained in the cells overproducing PKBα, but was not changed in the cells overexpressing PKCδ. In the CHO cell line overproducing both PKCδ and PKBα, H2O2-induced tyrosine phosphorylation of PKCδ was suppressed, and DNA fragmentation was diminished concomitantly. These results suggest that PKCδ contributes to H2O2-induced apoptosis by a mechanism independent of BAD and that PKCδ is a target of PKB for the regulation of cell survival.
影响因子：
56.9
作者：
L. Peso;M. González‐García;C. Page;R. Herrera;G. Núñez
通讯作者：
L. Peso;M. González‐García;C. Page;R. Herrera;G. Núñez
影响因子：
56.9
作者：
Cardone, MH;Roy, N;Reed, JC
通讯作者：
Reed, JC