Colletta G, Corda D, Schettini G, Cirafici A M, Kohn L D, Consiglio E
Dipartimento di Biologia e Patologia Cellulare e Molecolare, II Facoltà di Medicina e Chirurgia, Naples, Italy.
FEBS Lett. 1988 Feb 8;228(1):37-41. doi: 10.1016/0014-5793(88)80579-9.
The regulation of adenylate cyclase has been analyzed in normal rat thyroid cells as well as in the same cells transformed by the v-ras-k oncogene. In both cell types the adenylate cyclase complex consists of the two GTP-binding proteins, Gi and Gs, as demonstrated by the specific ADP-ribosylation induced by pertussis and cholera toxin, respectively. The response of adenylate cyclase of the transformed cells to forskolin, pertussis toxin and cholera toxin is attenuated with respect to the control cell line. The thyrotropic hormone (TSH), that acts on normal thyroid cells in culture as a growth factor by stimulating the adenylate cyclase activity, is not able to induce DNA synthesis nor does it stimulate adenylate cyclase in v-ras-k transformed cells.
已对正常大鼠甲状腺细胞以及经v-ras-k癌基因转化的相同细胞中的腺苷酸环化酶调节进行了分析。在这两种细胞类型中，腺苷酸环化酶复合物均由两种GTP结合蛋白Gi和Gs组成，分别由百日咳毒素和霍乱毒素诱导的特异性ADP核糖基化证明。与对照细胞系相比，转化细胞的腺苷酸环化酶对福斯可林、百日咳毒素和霍乱毒素的反应减弱。促甲状腺激素（TSH）在培养中作为生长因子作用于正常甲状腺细胞，通过刺激腺苷酸环化酶活性，但它不能诱导v-ras-k转化细胞中的DNA合成，也不能刺激腺苷酸环化酶。
