Nishizaki T, Matsuoka T, Nomura T, Sumikawa K
Department of Physiology, Kobe University School of Medicine, 7-5-1 Kusunoki-cho, Kobe, Chuo-ku, 650, Japan.
Biochem Biophys Res Commun. 1997 Sep 18;238(2):565-8. doi: 10.1006/bbrc.1997.7264.
A serum factor is recognized to interact with a protein kinase C (PKC) pathway. Indeed, treatment with fetal bovine serum enhanced ACh-evoked currents by PKC activation in the neuronal nicotinic ACh receptors (alpha7) and Torpedo ACh receptors expressed in Xenopus oocytes. In addition, potentiation of ACh-evoked currents induced by fetal bovine serum was observed also in the mutant Torpedo ACh receptors lacking potent PKC phosphorylation sites at Ser333 on the alpha subunit and Ser377 on the delta subunit; the potentiation was inhibited by the PKC inhibitor, PKC inhibitor peptide (PKCI), indicating that ACh receptor currents were enhanced by PKC activation but not by PKC phosphorylation of the receptors. On the other hand, fetal bovine serum enhanced kainate-evoked currents in oocytes expressing the alpha-amino3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, GluR1,3. The enhancement was not affected by the PKC inhibitors, PKCI or GF109203X, and instead, was inhibited by the Ca2+/calmodulin-dependent kinase II (CaMKII) inhibitor, KN-62. These results suggest that serum is not only involved in PKC activation but in CaMKII activation, and that thereby ACh receptor currents and AMPA receptor currents are each potentiated.
一种血清因子被认为可与蛋白激酶C（PKC）信号通路相互作用。实际上，用胎牛血清处理可通过激活PKC增强非洲爪蟾卵母细胞中表达的神经元烟碱型乙酰胆碱受体（α7）和电鳐乙酰胆碱受体的乙酰胆碱诱发电流。此外，在α亚基的Ser333和δ亚基的Ser377处缺乏有效PKC磷酸化位点的突变型电鳐乙酰胆碱受体中，也观察到胎牛血清诱导的乙酰胆碱诱发电流增强；该增强作用被PKC抑制剂PKC抑制肽（PKCI）抑制，表明乙酰胆碱受体电流是通过PKC激活而非受体的PKC磷酸化增强的。另一方面，胎牛血清增强了表达α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）受体GluR1、3的卵母细胞中的红藻氨酸诱发电流。该增强作用不受PKC抑制剂PKCI或GF109203X的影响，相反，被Ca2+/钙调蛋白依赖性激酶II（CaMKII）抑制剂KN-62抑制。这些结果表明，血清不仅参与PKC激活，还参与CaMKII激活，从而使乙酰胆碱受体电流和AMPA受体电流均得到增强。
