机译:Ste5支架蛋白的构象控制绝缘针对MAP激酶失活。
Department of Cellular and Molecular Pharmacology, University of California, San Francisco, 60016th Street, San Francisco, CA 94158, USA;
Department of Cellular and Molecular Pharmacology, University of California, San Francisco, 60016th Street, San Francisco, CA 94158, USA,Program in Biological Sciences, University of California, San Francisco, 600 16th Street, San Francisco, CA 94158, USA;
Banting and Best Department of Medical Research, Department of Molecular Genetics, and the Terrence Donnelly Center for Cellular and Biomolecular Research, University of Toronto, 160 College Street, Toronto, Ontario M5S 3E1, Canada;
Banting and Best Department of Medical Research, Department of Molecular Genetics, and the Terrence Donnelly Center for Cellular and Biomolecular Research, University of Toronto, 160 College Street, Toronto, Ontario M5S 3E1, Canada;
Department of Cellular and Molecular Pharmacology, University of California, San Francisco, 60016th Street, San Francisco, CA 94158, USA,Howard Hughes Medical Institute, University of California, San Francisco, 600 16th Street, San Francisco, CA 94158, USA;
机译:突变分析表明,酵母信息素应答丝裂原激活的蛋白激酶途径的激活涉及Ste5支架蛋白的构象变化
机译:丝裂素活化的蛋白激酶支架蛋白Ste5的核特异性和细胞周期调控的降解有助于信号传导能力的控制。
机译:结构决定因素的萌芽酵母支架蛋白Ste5的膜结合结构域的特异性:MAPK途径中支架蛋白在信号传导中的意义
机译:羧基蛋白蛋白质覆盖膜相关蛋白激酶的二聚化界面和磷酸化诱导的构象变化
机译:蛋白质相互作用在塑造MAP激酶激酶特性中的作用。
机译:在sTE5支架蛋白隔离对抗map激酶misactivation的构象控制
机译:突变分析表明,酵母的活化 信息素反应丝裂素激活蛋白激酶途径涉及。 Ste5支架蛋白的构象变化。