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George F. Crooke 《BMJ (Clinical research ed.)》1889,2(1510):1271-1272
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Michael J. Crooke J.G.T. Sneyd 《Biochimica et Biophysica Acta (BBA)/General Subjects》1980,631(1):40-48
Isolated hepatocytes converted exogenous [α-32P]ATP to cyclic [32P]AMP at high rates. This system was used for kinetic studies of the effects of glucagon, fluoride, free magnesium and free ATP4? on adenylate cyclase. In the absence or presence of glucagon, free Mg2+ activated adenylate cyclase by decreasing the Km for MgATP2? without changing V. Free ATP4? was not a potent inhibitor of adenylate cyclase and the only effect of glucagon was to increase V.Fluoride also increased the V of adenylate cyclase, but, in contrast to the results obtained with glucagon, the effect increased as the concentration of free Mg2+ increased. One explanation of the effect of fluoride, consistent with the idea that free Mg2+ activates adenylate cyclase and free ATP is not an inhibitor, is that fluoride increases the affinity of the enzyme for Mg2+. Weak inhibition of adenylate cyclase by ATP4? in the presence of fluoride cannot be excluded. 相似文献
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Stimulation of intracellular topoisomerase I activity by vasopressin and thrombin. Differential regulation by pertussis toxin. 下载免费PDF全文
Incubation of cultured rat aortic smooth muscle cells (A-10, ATCC CRL 1476) with [8-arginine]vasopressin (AVP) or thrombin increased the amount of DNA strand breakage induced by camptothecin, an inhibitor of topoisomerase I (DNA topoisomerase; EC 5.99.1.2) and transiently stimulated the extractable activity of this enzyme. Both topoisomerase-related responses were prevented by treatment of the cells with AVP or thrombin plus the appropriate receptor antagonist. The increase in strand breakage mediated by AVP and thrombin depended on the concentration of hormone. Neither AVP nor thrombin had any effect on strand breaks obtained with the epipodophyllotoxin VM-26, an inhibitor of topoisomerase II [DNA topoisomerase (ATP-hydrolysing); EC 5.99.1.3]. Pretreatment of the cells with pertussis toxin partially inhibited thrombin-mediated increases in camptothecin-induced strand breakage whereas AVP-mediated increases were unaffected. These results are consistent with the notion that AVP and thrombin induce a transient increase in intracellular topoisomerase I activity via interactions with their respective cell surface receptors and that the effects of the activation of these receptors are mediated by different G-proteins. 相似文献
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