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Hormonal regulation of Gi alpha level and adenylyl cyclase responsiveness.
Author(s) -
Reithmann C.,
Gierschik P.,
Werdan K.,
Jakobs KH
Publication year - 1990
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1990.tb05480.x
Subject(s) - adenylyl cyclase , gs alpha subunit , adcy10 , adcy9 , alpha (finance) , camp dependent pathway , g protein , endocrinology , g alpha subunit , medicine , adcy6 , stimulation , receptor , gi alpha subunit , hormone , chemistry , biology , protein subunit , biochemistry , gene , construct validity , nursing , patient satisfaction
Prolonged exposure of cells to adenylyl cyclase stimulatory hormonal factors can cause an increase in the level of membrane inhibitory G protein (Gi) alpha‐subunits, while inhibitory receptor agonists have been reported to induce the opposite response. As studied in cultured rat cardiomyocytes, the beta‐adrenoceptor‐induced increase in the level of Gi alpha proteins is protein synthesis‐dependent, is apparently not accompanied by an increase in G protein beta‐subunits and results in a decreased adenylyl cyclase responsiveness. On the other hand, a decrease in Gi alpha level apparently results in sensitization of adenylyl cyclase stimulation. These data suggest that the up‐ or down‐ regulation of the level and activity of Gi protein alpha‐subunits is a rather general cellular response, providing an intracellular negative feedback control against prolonged receptor activation.