Biochemical Properties of Hormone-Sensitive Adenylate Cyclase

Ross, Elliott M.; Gilman, Alfred G.

doi:10.1146/annurev.bi.49.070180.002533

Cited by 1,023 publications

(292 citation statements)

References 0 publications

Supporting

Mentioning

282

Contrasting

Unclassified

Order By: Relevance

“…A number of excellent reviews of this area have appeared [1][2][3]. As a prelude to a discussion of inhibition of adenylate cyclase it seems appropriate to present a brief perspective on stimulation of adenylate cyclase.…”

Section: Stimulation Of Adenylate Cyclasementioning

confidence: 99%

“…These and allied findings have led to the development of a general hypothesis, which proposes that hormone binding to receptors leads to the release of previously bound GDP (an ineffective stimulator), which allows occupancy by GTP and thus attainment of a more active R s • N s • C complex. On hydrolysis of GTP to GDP, the complex reverts to an inactive form, which coincides with the release of hormone [1][2][3].…”

Section: Stimulation Of Adenylate Cyclasementioning

confidence: 99%

See 1 more Smart Citation

Bimodal regulation of adenylate cyclase

Cooper

1982

FEBS Letters

161

View full text Add to dashboard Cite

Section: Stimulation Of Adenylate Cyclasementioning

confidence: 99%

Section: Stimulation Of Adenylate Cyclasementioning

confidence: 99%

Bimodal regulation of adenylate cyclase

Cooper

1982

FEBS Letters

161

View full text Add to dashboard Cite

“…Current research has demonstrated that mitogens such as serum, insulin, epidermal growth factor, platelet-derived growth factor or lectins all affect Ca*+ availability or mobilize cations in cells [29-401. In particular it appears likely that an amiloride-sensitive Na+/H+ antiport is activated by many mitogens causing Na+ to enter cells in exchange for H+ ions and provoking the subsequent exchange of intracellular Na+ for Ca*+ ions as occurs in other systems [33,36,41- Ca*+ could also decrease cyclic AMP availability by inhibiting adenylate cyclase or stimulating cyclic nucleotide phosphodiesterase which would further reduce the restraints exerted by cyclic AMP on growth [56,57]. These and other observations suggest that the intracellular (cytoplasmic?)…”

Section: Mitogens and Calciummentioning

confidence: 99%

Cyclic AMP, calcium and control of cell growth

Ralph

1983

FEBS Letters

View full text Add to dashboard Cite

The role of cyclic AMP and calcium in the control of normal and tumour cell growth is considered in relation to the question whether cyclic AMP is a true mitogen or cc-mitogen. It is proposed that cyclic AMP normally controls the cell cycle at a point in Gl phase only by virtue of its ability to exclude calcium required by cells to progress past this point into S phase. Therefore increased influx of calcium by other routes induced by various factors can bypass the inhibitory effect of cyclic AMP and stimulate growth. In these circumstances cyclic AMP or calcium may or may not facilitate further progress into S phase according to the metabolic requirements of individual cells. The relevance to cancer cells is considered. Cyclic AMP Calcium

show abstract

“…The apparent absolute dependence of yeast AC on Mn 2÷ both in situ (see above) and in vitro (where rates with 5 mM MgCI: alone are <3% of those with Mn 2+ [5]) is a puzzle, because it is unlikely that significant amounts of Mn 2÷ are available to AC in yeast ceils, although the vacuole can accumulate Mn 2÷ [14]. Mn 2÷ may short-circuit a yet unknown regulatory mechanism for yeast AC, as they appear to do for mammalian ACs [ 15]. This may explain why convincing effectors of yeast AC have not yet been found (several glucose metabolites have been screened; K. V., J. L., unpublished), though very high concentrations (0.1-0.25 M) of several sugars inhibit yeast AC by up to 35% in the presence of Mn 2÷ [16].…”

Section: Discussionmentioning

confidence: 99%