Premium
Down‐regulation of gonadotropin and β‐adrenergic receptors by hormones and cyclic AMP
Author(s) -
Fishman Peter H.,
Rebois R. Victor,
Zaremba Terrye
Publication year - 1985
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.240270305
Subject(s) - receptor , cyclase , cycloheximide , adenylate kinase , endocrinology , cholera toxin , medicine , agonist , growth hormone releasing hormone receptor , biology , gonadotropin , chemistry , hormone receptor , hormone , biochemistry , protein biosynthesis , cancer , breast cancer
Loss of gonadotropin receptors in murine Leydig tumor cells and of β‐adrenergic receptors in rat glioma C6 cells occurred following exposure of the cells to human chorionic gonadotropin and isoproterenol, respectively. Down‐regulation of receptors was mimicked in part by other agents that elevated cyclic AMP levels in the cells such as cholera toxin and dibutyryl cyclic AMP. Whereas agonist‐mediated receptor loss was rapid and almost total, down‐regulation by cyclic AMP was slower and less extensive. Down‐regulation of receptors did not appear to be accompanied by loss of the regulatory and catalytic components of adenylate cyclase. Hormone‐mediated down‐regulation was preceded by desensitization of hormone‐stimulated adenylate cyclase. In contrast, there was no evidence that cyclic AMP caused desensitization. Finally, loss of receptors induced either by agonists or cyclic AMP required protein synthesis as cycloheximide inhibited down‐regulation. We conclude that down‐regulation of receptors in these cells is a complex process involving both cyclic AMP‐independent and ‐dependent events.