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Fas凋亡途径的分子排序:Fas/APO-1蛋白酶Mch5是一种可被CrmA抑制的蛋白酶,它能激活多种Ced-3/ICE样半胱氨酸蛋白酶。

Molecular ordering of the Fas-apoptotic pathway: the Fas/APO-1 protease Mch5 is a CrmA-inhibitable protease that activates multiple Ced-3/ICE-like cysteine proteases.

作者信息

Srinivasula S M, Ahmad M, Fernandes-Alnemri T, Litwack G, Alnemri E S

机构信息

Department of Biochemistry and Molecular Pharmacology, Jefferson Medical College, Philadelphia, PA 19107, USA.

出版信息

Proc Natl Acad Sci U S A. 1996 Dec 10;93(25):14486-91. doi: 10.1073/pnas.93.25.14486.

Abstract

The Fas/APO-1-receptor associated cysteine protease Mch5 (MACH/FLICE) is believed to be the enzyme responsible for activating a protease cascade after Fas-receptor ligation, leading to cell death. The Fas-apoptotic pathway is potently inhibited by the cowpox serpin CrmA, suggesting that Mch5 could be the target of this serpin. Bacterial expression of proMch5 generated a mature enzyme composed of two subunits, which are derived from the pre-cursor proenzyme by processing at Asp-227, Asp-233, Asp-391, and Asp-401. We demonstrate that recombinant Mch5 is able to process/activate all known ICE/Ced-3-like cysteine proteases and is potently inhibited by CrmA. This contrasts with the observation that Mch4, the second FADD-related cysteine protease that is also able to process/activate all known ICE/Ced-3-like cysteine proteases, is poorly inhibited by CrmA. These data suggest that Mch5 is the most upstream protease that receives the activation signal from the Fas-receptor to initiate the apoptotic protease cascade that leads to activation of ICE-like proteases (TX, ICE, and ICE-relIII), Ced-3-like proteases (CPP32, Mch2, Mch3, Mch4, and Mch6), and the ICH-1 protease. On the other hand, Mch4 could be a second upstream protease that is responsible for activation of the same protease cascade in CrmA-insensitive apoptotic pathways.

摘要

Fas/APO-1受体相关的半胱氨酸蛋白酶Mch5(MACH/FLICE)被认为是在Fas受体连接后负责激活蛋白酶级联反应从而导致细胞死亡的酶。Fas凋亡途径受到牛痘丝氨酸蛋白酶抑制剂CrmA的强烈抑制,这表明Mch5可能是这种丝氨酸蛋白酶抑制剂的作用靶点。前体Mch5的细菌表达产生了一种由两个亚基组成的成熟酶,这两个亚基是通过在前体酶的Asp-227、Asp-233、Asp-391和Asp-401处进行加工而从该前体酶衍生而来的。我们证明重组Mch5能够加工/激活所有已知的ICE/Ced-3样半胱氨酸蛋白酶,并且受到CrmA的强烈抑制。这与以下观察结果形成对比:Mch4是第二种FADD相关的半胱氨酸蛋白酶,它也能够加工/激活所有已知的ICE/Ced-3样半胱氨酸蛋白酶,但受CrmA的抑制作用较弱。这些数据表明,Mch5是最上游的蛋白酶,它从Fas受体接收激活信号以启动凋亡蛋白酶级联反应,该级联反应导致ICE样蛋白酶(TX、ICE和ICE-relIII)、Ced-3样蛋白酶(CPP32、Mch2、Mch3、Mch4和Mch6)以及ICH-1蛋白酶的激活。另一方面,Mch4可能是第二种上游蛋白酶,它负责在对CrmA不敏感的凋亡途径中激活相同的蛋白酶级联反应。

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