Theoretical considerations concerning the effect of guanyl nucleotides on hormone-dependent adenylate cyclases show that the phenomena observed can be accounted for by postulating only one type of guanyl nucleotide regulatory site. The binding of GTP or of its non-hydrolizable analogues to the guanyl nucleotide regulatory site induces cyclase activation and may induce a decrease in agonist affinity towards the receptor. From basic principles it is shown that the potency ratio of guanyl nucleotides in inducing the decreased agonist affinity dose not necessarily reflect their order of affinities to the GTP regulatory site.
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