Hagiwara M, Ochiai M, Owada K, Tanaka T, Hidaka H
Department of Molecular and Cellular Pharmacology, Mie University School of Medicine, Japan.
J Biol Chem. 1988 May 5;263(13):6438-41.
The inhibitory effects of Ca2+-binding proteins on tyrosine phosphorylation of p36 protein isolated from bovine intestinal epithelium by immunoprecipitated p130fps were investigated. S-100 protein dose dependently inhibited the p36 phosphorylation, and calmodulin weakly depressed the phosphorylation, whereas parvalbumin and troponin C had no significant effects. The S-100 preparation purified from bovine brain did not contain phosphatase activity or ATPase activity. The concentration of ATP did not affect the S-100-mediated inhibition of phosphorylation but the substrate protein, p36, reversed the inhibition. S-100 similarly inhibited the tyrosine phosphorylation of p36 by p60src but did not affect the p36 phosphorylation by protein kinase C. S-100 inhibited the tyrosine kinase activity of p130fps using the other substrates tested as well. These results suggest that S-100 interacts with the substrate binding site of retroviral tyrosine-specific protein kinases and may play a regulatory role in the tyrosine phosphorylation.
研究了钙结合蛋白对通过免疫沉淀p130fps从牛肠上皮中分离出的p36蛋白酪氨酸磷酸化的抑制作用。S-100蛋白呈剂量依赖性抑制p36磷酸化,钙调蛋白微弱地抑制磷酸化,而小白蛋白和肌钙蛋白C则无显著作用。从牛脑中纯化的S-100制剂不含有磷酸酶活性或ATP酶活性。ATP的浓度不影响S-100介导的磷酸化抑制作用,但底物蛋白p36可逆转这种抑制作用。S-100同样抑制p60src对p36的酪氨酸磷酸化,但不影响蛋白激酶C对p36的磷酸化。S-100使用其他测试底物也抑制p130fps的酪氨酸激酶活性。这些结果表明,S-100与逆转录病毒酪氨酸特异性蛋白激酶的底物结合位点相互作用,可能在酪氨酸磷酸化中发挥调节作用。