Murachi T
Department of Clinical Science and Laboratory Medicine, Kyoto University, Faculty of Medicine, Japan.
Biochem Int. 1989 Feb;18(2):263-94.
Seven years have elapsed since the terms calpain and calpastatin were introduced. During these years, significant progress in research has been recorded. Thus, cloning and sequencing of cDNAs for calpains I and II and calpastatin have established amino acid sequences of these molecules. Structure-function relationship of calpastatin has been studied using mutated cDNAs expressed in E. coli. Interleukin 2 receptor-linked expression of calpastatin in HTLV-I-infected T-cells has been reported. Evidence for Ca2+-induced translocation of calpain to the cell membrane, followed by its autolytic activation, has been discussed. A great varieties of proteins such as several kinases, membrane and cytoskeletal proteins, and hormone receptors have been reported to be susceptible to calpains. This paper is to summarize our current knowledge on chemistry and biology of calpain and calpastatin and thereby to speculate the true function of calpains and their regulatory mechanisms.
自“钙蛋白酶”和“钙蛋白酶抑制蛋白”这两个术语被提出以来,已经过去了七年。在这些年里,研究取得了重大进展。因此,钙蛋白酶I和II以及钙蛋白酶抑制蛋白的cDNA克隆和测序确定了这些分子的氨基酸序列。利用在大肠杆菌中表达的突变cDNA研究了钙蛋白酶抑制蛋白的结构-功能关系。有报道称,在人嗜T细胞白血病病毒I型(HTLV-I)感染的T细胞中,钙蛋白酶抑制蛋白与白细胞介素2受体相关表达。已经讨论了钙离子诱导钙蛋白酶转移到细胞膜,随后发生自溶激活的证据。据报道,多种蛋白质,如几种激酶、膜蛋白和细胞骨架蛋白以及激素受体,都易受钙蛋白酶的作用。本文旨在总结我们目前关于钙蛋白酶和钙蛋白酶抑制蛋白的化学和生物学知识,从而推测钙蛋白酶的真正功能及其调节机制。