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蛋白激酶C抑制通过激活中性鞘磷脂酶诱导细胞凋亡和神经酰胺生成。

Protein kinase C inhibition induces apoptosis and ceramide production through activation of a neutral sphingomyelinase.

作者信息

Chmura S J, Nodzenski E, Weichselbaum R R, Quintans J

机构信息

Department of Pathology, Division of Biological Sciences, University of Chicago, Illinois, USA.

出版信息

Cancer Res. 1996 Jun 15;56(12):2711-4.

PMID:8665499
Abstract

We report that WEHI-231 undergo apoptosis following exposure to the protein kinase C inhibitors chelerythrine chloride and calphostin C. Following the addition of chelerythrine or calphostin C to WEHI-231 cells, ceramide production increased over baseline levels with a concurrent decrease in sphingomyelin. More detailed examinations determined that the ceramide accumulation resulted from activation of neutral, but not acidic, sphingomyelinase. These results suggest an antagonistic relationship between protein kinase C activity and ceramide in the signaling events preceding apoptosis.

摘要

我们报告称,WEHI-231细胞在暴露于蛋白激酶C抑制剂氯化白屈菜红碱和钙磷蛋白C后会发生凋亡。在向WEHI-231细胞中添加氯化白屈菜红碱或钙磷蛋白C后,神经酰胺的产生量超过基线水平,同时鞘磷脂减少。更详细的研究确定,神经酰胺的积累是由中性而非酸性鞘磷脂酶的激活引起的。这些结果表明,在凋亡之前的信号事件中,蛋白激酶C活性与神经酰胺之间存在拮抗关系。

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