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缺乏母细胞素(P19)的小鼠的正常发育,母细胞素是一种与细胞周期调控有关的磷蛋白。

Normal development of mice lacking metablastin (P19), a phosphoprotein implicated in cell cycle regulation.

作者信息

Schubart U K, Yu J, Amat J A, Wang Z, Hoffmann M K, Edelmann W

机构信息

Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461, USA.

出版信息

J Biol Chem. 1996 Jun 14;271(24):14062-6. doi: 10.1074/jbc.271.24.14062.

DOI:10.1074/jbc.271.24.14062
PMID:8662897
Abstract

Metablastin, also called P19, stathmin, prosolin, Lap18, and oncoprotein18, is a highly conserved cytosolic protein that undergoes extracellular factor- and cell cycle-regulated serine phosphorylation and developmentally regulated expression in mammals. It has been implicated in a variety of cellular functions including growth and differentiation, and recent evidence suggests an involvement in cell cycle control. To explore its potential role in mammalian development, we have disrupted the gene encoding metablastin by gene targeting in mice. The metablastin null mutants have no overt phenotype regarding development, growth rate, behavior, T cell maturation, or fertility and do not exhibit an increased predisposition to tumors. SCG10, a protein closely related in structure to metablastin, shows no compensatory up-regulation in metablastin-/- mice. Although the data suggest that metablastin is not essential for mammalian development, the knockout mice should prove valuable in exploring the role of this protein in cell cycle regulation.

摘要

变构菌素,也被称为P19、微管相关蛋白、前溶胶蛋白、Lap18和癌蛋白18,是一种高度保守的胞质蛋白,在哺乳动物中会经历细胞外因子和细胞周期调控的丝氨酸磷酸化以及发育调控的表达。它与多种细胞功能有关,包括生长和分化,最近的证据表明它参与细胞周期控制。为了探索其在哺乳动物发育中的潜在作用,我们通过基因打靶在小鼠中破坏了编码变构菌素的基因。变构菌素基因敲除突变体在发育、生长速度、行为、T细胞成熟或生育能力方面没有明显的表型,也没有表现出肿瘤易感性增加。SCG10是一种在结构上与变构菌素密切相关的蛋白质,在变构菌素基因敲除小鼠中没有显示出补偿性上调。尽管数据表明变构菌素对哺乳动物发育不是必需的,但基因敲除小鼠在探索这种蛋白质在细胞周期调控中的作用方面应该是有价值的。

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Normal development of mice lacking metablastin (P19), a phosphoprotein implicated in cell cycle regulation.缺乏母细胞素(P19)的小鼠的正常发育,母细胞素是一种与细胞周期调控有关的磷蛋白。
J Biol Chem. 1996 Jun 14;271(24):14062-6. doi: 10.1074/jbc.271.24.14062.
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