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一种23 kDa应激诱导的小鼠腹腔巨噬细胞蛋白的克隆与特性分析

Cloning and characterization of a 23-kDa stress-induced mouse peritoneal macrophage protein.

作者信息

Ishii T, Yamada M, Sato H, Matsue M, Taketani S, Nakayama K, Sugita Y, Bannai S

机构信息

Department of Biochemistry, University of Tsukuba, Ibaraki, Japan.

出版信息

J Biol Chem. 1993 Sep 5;268(25):18633-6.

PMID:8360158
Abstract

Exposure of mouse peritoneal macrophages to oxidative and sulfhydryl-reactive agents in vitro enhances synthesis of a few cellular proteins that may be important in a self-defense system. A cDNA encoding a novel stress-inducible protein, designated MSP23 (macrophage 23-kDa stress protein), was cloned from a cDNA library of the macrophages by differential screening. A 1.0-kilobase mRNA transcript hybridized with the MSP23 cDNA gradually increased in macrophages upon culture in vitro. Treatment with diethylmaleate or glucose/glucose oxidase, which generates H2O2, markedly enhanced the induction of the transcript after several hours. Cadmium chloride and sodium arsenite also induced the transcript. An antiserum raised against recombinant MSP23 reacted with the 23-kDa stress-inducible protein of the macrophages. The amounts of 23-kDa protein in the cells rapidly increased during culture with diethylmaleate. The mRNA was detected in various tissues, and it was especially high in content in the liver. A search of databases revealed that six proteins of various species from bacteria to the mouse have a sequence homology to MSP23. One of the proteins is the C22 component of alkyl hydroperoxide reductase, which is induced by hydrogen peroxide in Salmonella typhimurium.

摘要

在体外将小鼠腹腔巨噬细胞暴露于氧化和巯基反应性试剂中,可增强一些细胞蛋白质的合成,这些蛋白质可能在自我防御系统中起重要作用。通过差异筛选从巨噬细胞的cDNA文库中克隆了一个编码新型应激诱导蛋白的cDNA,命名为MSP23(巨噬细胞23 kDa应激蛋白)。与MSP23 cDNA杂交的1.0千碱基mRNA转录本在巨噬细胞体外培养时逐渐增加。用马来酸二乙酯或葡萄糖/葡萄糖氧化酶(产生H2O2)处理,数小时后显著增强了转录本的诱导。氯化镉和亚砷酸钠也诱导了该转录本。针对重组MSP23产生的抗血清与巨噬细胞的23 kDa应激诱导蛋白发生反应。在用马来酸二乙酯培养期间,细胞中23 kDa蛋白的量迅速增加。在各种组织中都检测到了该mRNA,其中肝脏中的含量特别高。数据库搜索显示,从细菌到小鼠的各种物种的六种蛋白质与MSP23具有序列同源性。其中一种蛋白质是烷基过氧化氢还原酶的C22组分,它在鼠伤寒沙门氏菌中由过氧化氢诱导产生。

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