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蛋白酶体抑制剂增强肿瘤坏死因子处理的U937细胞中类CPP32的活性。

Enhancement of CPP32-like activity in the TNF-treated U937 cells by the proteasome inhibitors.

作者信息

Fujita E, Mukasa T, Tsukahara T, Arahata K, Omura S, Momoi T

机构信息

Division of Development and Differentiation, NCNP, Tokyo, Japan.

出版信息

Biochem Biophys Res Commun. 1996 Jul 5;224(1):74-9. doi: 10.1006/bbrc.1996.0986.

Abstract

CPP32, which is most closely related to CED-3 in the apoptotic protease in C. elegance, is activated during apoptosis induced by anti-Fas and TNF. Since processing of CPP32 is important for the activation, we examined the effects of protease inhibitors on CPP32-like activity in the TNF-treated U937 cells. Unexpectedly, proteasome inhibitors (at 5 microM) such as Z-LLnV, Z-LLL, and lactacystin enhanced CPP32-like activity, Ac-DEVD-MCA degrading activity, in the TNF-treated U937 cells in 3 hr, but E64d, cysteine protease inhibitor, did not. These proteasome inhibitors alone did not enhance CPP32-like activity in the untreated U937 cells under the condition used. The proteasome seems to protect the cells from apoptosis by degrading CPP32-like protease or its processing enzyme.

摘要

CPP32与秀丽隐杆线虫凋亡蛋白酶中与CED-3关系最为密切的蛋白酶相关,在抗Fas和TNF诱导的凋亡过程中被激活。由于CPP32的加工对于激活很重要,我们研究了蛋白酶抑制剂对经TNF处理的U937细胞中CPP32样活性的影响。出乎意料的是,蛋白酶体抑制剂(5 microM)如Z-LLnV、Z-LLL和乳胞素在3小时内增强了经TNF处理的U937细胞中的CPP32样活性,即Ac-DEVD-MCA降解活性,但半胱氨酸蛋白酶抑制剂E64d没有。在所使用的条件下,这些蛋白酶体抑制剂单独并不会增强未处理的U937细胞中的CPP32样活性。蛋白酶体似乎通过降解CPP32样蛋白酶或其加工酶来保护细胞免受凋亡。

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