Okumura-Noji K, Kato T, Tanaka R
Department of Biochemistry, Nagoya City University Medical School, Japan.
Neurochem Res. 1986 Nov;11(11):1583-95. doi: 10.1007/BF00965777.
Endogenous protein phosphorylation of PC12 cells was investigated with the homogenate as well as intact cells. In the case of the homogenate, the major proteins that were phosphorylated in the presence of Ca2+ were found to be of Mr 95 K and Mr 50 K-55 K. Ca2+/calmodulin-dependent protein kinase appeared to be responsible for phosphorylation of Mr 50 K-55 K proteins and partly of Mr 95 K protein. The apparent Km's for Ca2+ of Mr 95 K and 50 K-55 K protein phosphorylation were 2.2 x 10(-7) M and around 1.5 x 10(-6) M, respectively. Since several cell lines of neuroblastoma exhibited Mr 95 K protein phosphorylation of similar type, the protein phosphorylation may be a common process shared by neuronal cells. Depolarization of intact PC12 cells by high K+ concentrations induced Mr 95 K protein phosphorylation. The results suggest that a physiological increase by excitation in the intracellular Ca2+ concentration triggers phosphorylation of Mr 95 K protein in neuronal cells and this phosphorylation may play a role in the regulation of transmitter release.
利用匀浆以及完整细胞对PC12细胞的内源性蛋白质磷酸化进行了研究。对于匀浆,发现在Ca2+存在下被磷酸化的主要蛋白质的分子量为95K和50K - 55K。Ca2+/钙调蛋白依赖性蛋白激酶似乎负责50K - 55K蛋白质以及部分95K蛋白质的磷酸化。95K和50K - 55K蛋白质磷酸化的Ca2+表观Km值分别为2.2×10(-7)M和约1.5×10(-6)M。由于几种神经母细胞瘤细胞系表现出类似类型的95K蛋白质磷酸化,蛋白质磷酸化可能是神经元细胞共有的一个常见过程。高K+浓度使完整的PC12细胞去极化会诱导95K蛋白质磷酸化。结果表明,细胞内Ca2+浓度因兴奋而发生的生理性升高会触发神经元细胞中95K蛋白质的磷酸化,并且这种磷酸化可能在递质释放的调节中起作用。