Aktories K, Schultz G, Jakobs K H
Biochim Biophys Acta. 1982 Oct 28;719(1):58-64. doi: 10.1016/0304-4165(82)90307-5.
The influence of cholera toxin on hormonal inhibition of adenylate cyclase and concomitant stimulation of low Km GTPase was studied in adipocyte membrane preparations. In hamster adipocyte ghosts, cholera toxin caused an about 8-fold activation of the adenylate cyclase. The antilipolytic hormonal factors, prostaglandin E1 (1 micro M), N6-phenylisopropyladenosine (1 micro M) and nicotinic acid (30 micro M) reduced both basal and cholera toxin-stimulated enzyme activities. Similar data with regard to inhibition of cholera toxin-stimulated adenylate cyclase were obtained in mouse and rat adipocyte ghosts. As studied in hamster adipocyte ghosts, prostaglandin E1 (1 micro M) increased GTP hydrolysis by a low Km GTPase by about 3-4 fold. Pretreatment of the membrane preparation with cholera toxin did not impair prostaglandin E1-induced GTPase stimulation. The data suggest that cholera toxin does not directly affect the GTPase enzyme stimulated by adenylate cyclase inhibitory hormones.
在脂肪细胞膜制剂中研究了霍乱毒素对激素抑制腺苷酸环化酶以及同时刺激低 Km GTP 酶的影响。在仓鼠脂肪细胞空壳中,霍乱毒素使腺苷酸环化酶激活约 8 倍。抗脂解激素因子前列腺素 E1(1 μM)、N6-苯异丙基腺苷(1 μM)和烟酸(30 μM)降低了基础和霍乱毒素刺激的酶活性。在小鼠和大鼠脂肪细胞空壳中获得了关于抑制霍乱毒素刺激的腺苷酸环化酶的类似数据。如在仓鼠脂肪细胞空壳中所研究的,前列腺素 E1(1 μM)使低 Km GTP 酶的 GTP 水解增加约 3 - 4 倍。用霍乱毒素预处理膜制剂并不损害前列腺素 E1 诱导的 GTP 酶刺激。数据表明霍乱毒素不直接影响由腺苷酸环化酶抑制激素刺激的 GTP 酶。