FEBS Letters | |
Regulation of adenylate cyclase by hormones and G‐proteins | |
Levitzki, Alexander1  | |
[1] Department of Biological Chemistry, Institute of Life Sciences, The Hebrew University of Jerusalem, 91904 Jerusalem, Israel | |
关键词: G-protein; Adenylate cyclase; Receptor; | |
DOI : 10.1016/0014-5793(87)81419-9 | |
学科分类:生物化学/生物物理 | |
来源: John Wiley & Sons Ltd. | |
【 摘 要 】
Over the past few years, it has become apparent that a large number of transmembrane signaling systems operate through heterotrimeric G-proteins ([1] Gilman, A.G. (1984) Cell 36, 577-579; [2] Baker, P.F. (1986) Nature 320, 395). Adenylate cyclase is regulated by stimulatory hormones through Gs(αsβγ) and inhibitory hormones through Gi(αiβγ) ([2]; Katada, T. et al. (1984) J. Biol. Chem. 259, 3586-3595), whereas the breakdown of phosphatidylinositol bisphosphate (PIP2) to inositol trisphosphate (IP3) and diacylglycerol (DG) by phospholipase C is probably also mediated by a heterotrimeric G-protein (Go or Gi) [1,2]. Similarly, the activation of cGMP phosphodiesterase by light-activated rhodopsin is mediated through the heterotrimeric G-protein transducin (Stryer, L. (1986) Rev. Neurosci. 9, 89-119). Other transmembrane signaling systems may also be found to involve G-proteins similar to those already recognized. Because of the emerging universality of G-proteins as transducers of receptor-triggered signals, it may be useful to evaluate the current models prevailing in the adenylate cyclase field, as these models seem to guide our way in evaluating the role of G-proteins in transmembrane signaling, in general.
【 授权许可】
Unknown
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