Borowski P, Medem S, Laufs R, Weber W
Institut für Medizinische Mikrobiologie und Immunologie, Universitaetsklinik Eppendorf, Federal Republic of Germany.
J Biochem. 1994 May;115(5):825-9. doi: 10.1093/oxfordjournals.jbchem.a124423.
We investigated polyionic agents with regard to their effects as modulators of epidermal growth factor receptor (EGF-R) kinase activity. Many synthetic polypeptides containing glutamine as well as casein were phosphorylated, while polycationic compounds with tyrosine residues were not phosphorylatable and thus inhibited the EGF-R activity. Polyarginine, protamine sulfate, spermidine, heparin, and poly-L-lysine with a chain length of < 20.5 kDa triggered the phosphorylation of poly(Tyr1, Glu4). On the other hand, dextran sulfate and poly-L-lysine with chain lengths of > 20.5 kDa inhibited the EGF-R kinase activity. Alteration of the state of autophosphorylation of EGF-R is not in agreement with the activity of EGF-R kinase towards poly(Tyr1, Glu4). Casein and histone H1 both increased the autophosphorylation of EGF-R in a concentration-dependent manner, but only casein increased the activity of the enzyme towards an exogenous substrate. The compounds enhancing the EGF-R activity, such as poly-L-lysine, protamine, and poly-L-arginine, down-modulated the autophosphorylation reaction. We discuss the consequences of these effects as to in vivo conditions.
我们研究了聚离子型试剂作为表皮生长因子受体（EGF-R）激酶活性调节剂的作用。许多含谷氨酰胺的合成多肽以及酪蛋白都被磷酸化，而含酪氨酸残基的聚阳离子化合物则不可磷酸化，因此抑制了EGF-R活性。多聚精氨酸、硫酸鱼精蛋白、亚精胺、肝素以及链长<20.5 kDa的聚-L-赖氨酸引发了聚（Tyr1，Glu4）的磷酸化。另一方面，链长>20.5 kDa的硫酸葡聚糖和聚-L-赖氨酸抑制了EGF-R激酶活性。EGF-R自身磷酸化状态的改变与EGF-R激酶对聚（Tyr1，Glu4）的活性不一致。酪蛋白和组蛋白H1均以浓度依赖的方式增加了EGF-R的自身磷酸化，但只有酪蛋白增加了该酶对外源底物的活性。增强EGF-R活性的化合物，如聚-L-赖氨酸、鱼精蛋白和聚-L-精氨酸，下调了自身磷酸化反应。我们讨论了这些作用对体内条件的影响。
