Platts E A, Schulster D, Cooke B A
Department of Biochemistry and Chemistry, Royal Free Hospital School of Medicine, London, U.K.
Biochem J. 1988 Aug 1;253(3):895-9. doi: 10.1042/bj2530895.
Luteinizing-hormone (LH)-stimulated cyclic AMP production in rat testis Leydig cells was desensitized by both LH and 12-O-tetradecanoylphorbol 13-acetate (TPA). However, TPA, but not LH, enhanced the subsequent response to cholera toxin. Treatment of the cells with pertussis toxin potentiated cyclic AMP production in both control and LH-desensitized cells, but did not potentiate further the responses obtained by TPA pretreatment. The results implicate the presence of an inhibitory GTP-binding protein (Gi), which may be inhibited by TPA. The presence of a Gi-like protein within the plasma membrane of Leydig cells was demonstrated by pertussis-toxin-catalysed [32P]ADP-ribosylation of a Mr-40000-41000 protein.
促黄体生成素（LH）刺激大鼠睾丸间质细胞产生环磷酸腺苷（cAMP）的过程会被LH和十四酰佛波醇乙酯（TPA）脱敏。然而，TPA而非LH增强了随后对霍乱毒素的反应。用百日咳毒素处理细胞会增强对照细胞和LH脱敏细胞中环磷酸腺苷的产生，但不会进一步增强TPA预处理所获得的反应。结果表明存在一种抑制性GTP结合蛋白（Gi），它可能被TPA抑制。通过百日咳毒素催化的Mr-40000-41000蛋白的[32P]ADP核糖基化，证明了间质细胞质膜内存在一种类似Gi的蛋白。
