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肌动蛋白分子上尖端部结构域的肌动蛋白激酶磷酸化作用。

Phosphorylation by actin kinase of the pointed end domain on the actin molecule.

作者信息

Furuhashi K, Hatano S, Ando S, Nishizawa K, Inagaki M

机构信息

Department of Molecular Biology, School of Science, Nagoya University, Japan.

出版信息

J Biol Chem. 1992 May 5;267(13):9326-30.

PMID:1315751
Abstract

Fragmin from plasmodium of Physarum polycephalum binds G-actin and severs F-actin in the presence of Ca2+ over 10(-6) M. The fragmin-actin complex consisting of fragmin and G-actin nucleates actin polymerization and caps the barbed (fast growing) end of F-actin, regardless of the concentrations of Ca2+, and the actin filaments are shortened. Actin kinase purified from plasmodium abolishes the nucleation and capping activities of the complex by phosphorylating actin of the fragmin-actin complex (Furuhashi, K., and Hatano, S. (1990) J. Cell. Biol. 111, 1081-1087). This inactivation of the complex leads to production of long actin filaments. We obtained evidence that Physarum actin is phosphorylated by actin kinase at Thr-201, and probably at Thr-202 and/or Thr-203, with 1 mol of phosphate distributed among them. This finding raises the possibility that the site of phosphorylation, Thr-201 to Thr-203, is positioned on the pointed (slow growing) end domain of the actin molecule, because growth of actin filaments from the fragmin-actin complex occurs only from the pointed end. These observations are consistent with a model of the three-dimensional structure of G-actin. Inactivation of the fragmen-actin complex may follow phosphorylation of the pointed end domain of actin.

摘要

多头绒泡菌疟原虫的凝溶胶蛋白在钙离子浓度超过10⁻⁶ M时可结合G-肌动蛋白并切断F-肌动蛋白。由凝溶胶蛋白和G-肌动蛋白组成的凝溶胶蛋白-肌动蛋白复合物可引发肌动蛋白聚合,并封闭F-肌动蛋白的带刺(快速生长)末端,而不受钙离子浓度的影响,且肌动蛋白丝会缩短。从疟原虫中纯化出的肌动蛋白激酶通过磷酸化凝溶胶蛋白-肌动蛋白复合物中的肌动蛋白,消除了该复合物的成核和封闭活性(古桥克、波多野修,(1990年)《细胞生物学杂志》111卷,第1081 - 1087页)。该复合物的这种失活导致长肌动蛋白丝的产生。我们获得的证据表明,多头绒泡菌肌动蛋白在苏氨酸-201处被肌动蛋白激酶磷酸化,可能在苏氨酸-202和/或苏氨酸-203处也被磷酸化,1摩尔磷酸分布在这些位点之间。这一发现增加了磷酸化位点苏氨酸-201至苏氨酸-203位于肌动蛋白分子的钝端(缓慢生长)结构域的可能性,因为从凝溶胶蛋白-肌动蛋白复合物中生长的肌动蛋白丝仅从钝端开始。这些观察结果与G-肌动蛋白三维结构模型一致。凝溶胶蛋白-肌动蛋白复合物的失活可能是由于肌动蛋白钝端结构域的磷酸化所致。

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