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1 ty of the mutant form of Gsalpha to regulate adenylylcyclase.
2 r content of cAMP generated by activation of adenylylcyclase (AC) through the beta-adrenergic recepto
3 r content of cAMP generated by activation of adenylylcyclase (AC; EC 4.6.1.1) is a key determinant of
4 evels of G protein alpha subunits regulating adenylylcyclase activity (Gs alpha-both 45- and 52-kDa f
5 (1) beta 1-mRNA and receptor expression and adenylylcyclase activity and (2) beta 1-mRNA and recepto
6 gnificant attenuation of SKF81297-stimulated adenylylcyclase activity in D(1) dopamine receptor-expre
7 s showed no reduction of SKF81297-stimulated adenylylcyclase activity in D(5) dopamine receptor-expre
8 eceptors, particularly at the mRNA level, or adenylylcyclase activity in isolated cardiac myocytes ex
9 e of the gamma7 subunit in the regulation of adenylylcyclase activity in response to isoproterenol.
10 A and receptor expression but does not alter adenylylcyclase activity stimulated at either the recept
13 ne receptor, G protein gamma(7) subunit, and adenylylcyclase are selectively expressed in the striatu
14 4)/Gsalpha produced a chimera that activated adenylylcyclase but abolished progression to primitive e
15 signaling of beta2-adrenergic receptors from adenylylcyclase coupling to the mitogen-activated protei
16 beta 1-mRNA and receptor downregulation and adenylylcyclase desensitization in response to isoproter
17 beta 1-mRNA and receptor downregulation and adenylylcyclase desensitization induced by prolonged nor
20 recognized that the beta-adrenergic receptor-adenylylcyclase system is altered during myocardial isch
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