Hoshijima M, Ueda T, Hamamori Y, Ohmori T, Takai Y
Department of Biochemistry, Kobe University School of Medicine, Japan.
Biochem Biophys Res Commun. 1988 Apr 15;152(1):285-93. doi: 10.1016/s0006-291x(88)80712-5.
Incubation of the serum-deprived cultures of NIH/3T3 cells with bombesin or platelet-derived growth factor (PDGF) induced the phospholipase C-mediated hydrolysis of phosphoinositides. Protein kinase C-activating 12-O-tetradecanoylphorbol 13-acetate (TPA) and pertussis toxin inhibited the bombesin-induced phospholipase C reactions. AlF4-, a direct activator of GTP-binding proteins (G proteins), also induced the phospholipase C reactions and TPA inhibited the AlF4- -induced reactions. These results suggest that a pertussis toxin-sensitive G protein is involved in the coupling of the bombesin receptor to the phospholipase C and that the coupling of the G protein to the phospholipase C is inhibited by protein kinase C. In contrast, neither TPA nor pertussis toxin inhibited the PDGF-induced phospholipase C reactions, indicating that a pertussis toxin-sensitive G protein is not involved in the coupling of the PDGF receptor to the phospholipase C and that this coupling is insensitive to protein kinase C. These results suggest that the regulatory mechanism of the PDGF receptor for the phospholipase C activation is different from that of the bombesin receptor.
用铃蟾肽或血小板衍生生长因子（PDGF）处理血清饥饿培养的NIH/3T3细胞，可诱导磷脂酶C介导的磷酸肌醇水解。蛋白激酶C激活剂12 - O - 十四烷酰佛波醇13 - 乙酸酯（TPA）和百日咳毒素可抑制铃蟾肽诱导的磷脂酶C反应。GTP结合蛋白（G蛋白）的直接激活剂AlF4 - 也可诱导磷脂酶C反应，且TPA可抑制AlF4 - 诱导的反应。这些结果表明，一种对百日咳毒素敏感的G蛋白参与了铃蟾肽受体与磷脂酶C的偶联，并且G蛋白与磷脂酶C的偶联受到蛋白激酶C的抑制。相比之下，TPA和百日咳毒素均未抑制PDGF诱导的磷脂酶C反应，这表明对百日咳毒素敏感的G蛋白不参与PDGF受体与磷脂酶C的偶联，且这种偶联对蛋白激酶C不敏感。这些结果表明，PDGF受体激活磷脂酶C的调节机制与铃蟾肽受体不同。
