G protein regulation of adenylate cyclase

Article Abstract:

Recent advances in knowledge on the regulation of adenylate cyclase (AC) by G proteins are described. AC combines negative and positive signals that act through G protein-coupled cell-surface receptors with other extracellular stimuli to regulate levels of cAMP within the cell. In 1997, Hurley and his associates determined the crystal structure of its catalytic core while Tesmer discovered the complex containing the cyclase catalytic domains bound to an active conformation of the cyclase-stimulating G protein alpha-subunit.

Adenylate cyclase

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Receptor sites for Ca2+ channel antagonists

Article Abstract:

The L-type Ca2+ channels found in smooth and cardiac muscles contain receptor sites susceptible to either dihydropyridine or phenylalkylamine modulation. These binding sites promote high conservation in the Ca2+ channel alpha1 subunits involving Ca2+ channel antagonist reactions resulting in therapeutic effects. Moreover, results indicate that phenylalkylamine hinders Ca2+ ion movement via pore-blocking while dihydropyridine functions via extracellular gating alterations.

Research, Somatotropin, Dioxin, Dioxins, Carcinogens, Steroid hormones, Steroid receptors, Calcium channel blockers, Genetic toxicology, Transduction, Transduction (Genetics), Somatotropin receptors

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Direct regulation of cardiac Ca2+ channels by G proteins: neither proven nor necessary?

Article Abstract:

G proteins have been found to affect the activity of cardiac L-type calcium (Ca2+) channels. Experimental studies confirm the action of G proteins on Ca2+ channels in excised patches and artificial lipid bilayers. Similarly, these studies have determined that G proteins bind to purified Ca2+ channels and influence dihydropyridine affinity to Ca2+ channels. However, the physiological effects caused by the G protein mechanism lack immediate biological importance.

Phosphorylation, Isoproterenol

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