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ICE/CED3样蛋白酶作为控制异常凋亡的治疗靶点。

ICE/CED3-like proteases as therapeutic targets for the control of inappropriate apoptosis.

作者信息

Nicholson D W

机构信息

Department of Biochemistry and Molecular Biology, Merck Frosst Centre for Therapeutic Research, Pointe Claire-Dorval, Quebec, Canada.

出版信息

Nat Biotechnol. 1996 Mar;14(3):297-301. doi: 10.1038/nbt0396-297.

DOI:10.1038/nbt0396-297
PMID:9630889
Abstract

Excessive or failed apoptosis is a prominent morphological feature of several human diseases. Many of the key biochemical players that contribute to the highly ordered process of apoptotic cell death have recently been identified. These include members of the emerging family of cysteine proteases related to mammalian interleukin-1 beta converting enzyme (ICE) and to CED-3, the product of a gene that is necessary for programmed cell death in the nematode C. elegans. Among a growing number of potential molecular targets for the control of human diseases where inappropriate apoptosis is prominent, ICE/CED-3-like proteases may be an attractive and tangible point for therapeutic intervention.

摘要

细胞凋亡过度或失败是多种人类疾病的一个显著形态学特征。最近已鉴定出许多促成细胞凋亡性死亡这一高度有序过程的关键生化因子。这些因子包括与哺乳动物白细胞介素-1β转化酶(ICE)以及与线虫秀丽隐杆线虫程序性细胞死亡所必需基因的产物CED-3相关的新兴半胱氨酸蛋白酶家族成员。在越来越多以不适当细胞凋亡为突出特征的人类疾病的潜在分子靶点中,ICE/CED-3样蛋白酶可能是治疗干预的一个有吸引力且切实可行的切入点。

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ICE/CED3-like proteases as therapeutic targets for the control of inappropriate apoptosis.ICE/CED3样蛋白酶作为控制异常凋亡的治疗靶点。
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