Matsuoka T, Nishizaki T, Ikeuchi Y
Department of Public Health, Kobe University School of Medicine, Japan.
Biochem Biophys Res Commun. 1996 Jan 17;218(2):633-7. doi: 10.1006/bbrc.1996.0112.
Fetal bovine serum evoked Ca(2+)-dependent chloride currents with two components in Xenopus oocytes. The evoked currents were inhibited by GDP beta S, but not by pertussis toxin (PTX). An inositol 1,4,5-triphosphate (IP3) receptor antagonist, heparin completely inhibited the currents, although a phospholipase C inhibitor, neomycin had no effect. The serum-activated currents were enhanced to 171% by a selective protein kinase C (PKC) inhibitor, GF109203X. By contrast, a potent PKC activator, TPA, abolished the initial component of the currents and arachidonic acid enhanced this effect. The effects of TPA and/or arachidonic acid on the currents inhibited by GF109203X. These results indicate that the receptor for serum is linked to a PTX-insensitive G-protein involving cytosolic Ca2+ release through IP3 and PKC activation by a mechanism independent of a phospholipase C-mediated phospholipid signaling. Furthermore, the evoked currents are regulated by PKC and arachidonic acid appears to potentiate its effect.
胎牛血清在非洲爪蟾卵母细胞中诱发了具有两个成分的钙依赖性氯电流。诱发的电流被GDPβS抑制，但不被百日咳毒素（PTX）抑制。肌醇1,4,5-三磷酸（IP3）受体拮抗剂肝素完全抑制了电流，尽管磷脂酶C抑制剂新霉素没有作用。血清激活的电流被选择性蛋白激酶C（PKC）抑制剂GF109203X增强至171%。相比之下，一种有效的PKC激活剂佛波酯（TPA）消除了电流的初始成分，花生四烯酸增强了这种作用。TPA和/或花生四烯酸对被GF109203X抑制的电流有影响。这些结果表明，血清受体与一种对PTX不敏感的G蛋白相连，该G蛋白通过IP3涉及胞质钙释放，并通过一种独立于磷脂酶C介导的磷脂信号传导的机制激活PKC。此外，诱发的电流受PKC调节，花生四烯酸似乎增强了其作用。
