New perspectives in cAMP-signaling modulation.

Abstract : Cyclic adenosine 3',5'-monophosphate (cAMP) mediates the biological effects of various hormones and neurotransmitters. Stimulation of cardiac β-adrenergic receptors (β-AR) via catecholamines leads to activation of adenylyl cyclases and increases cAMP production to enhance myocardial function. Because many other receptors signaling through cAMP generation exist in cardiac myocytes, a central question is how different hormones induce distinct cellular responses through the same second messenger. A large body of evidence suggests that the localization and compartmentalization of β-AR/cAMP signaling affects the net outcome of biological functions. Spatiotemporal dynamics of cAMP action is achieved by various proteins, including protein kinase A (PKA), phosphodiesterases, and scaffolding proteins such as A-kinase-anchoring proteins. In addition, the discovery of the cAMP target Epac (exchange proteins directly activated by cAMP), which functions in a PKA-independent manner, represents a novel mechanism for governing cAMP-signaling specificity. Aberrant cAMP signaling through dysregulation of β-AR/cAMP compartmentalization may contribute to cardiac remodeling and heart failure.
Type de document :
Article dans une revue
Curr Heart Fail Rep, 2011, 8 (3), pp.159-67. 〈10.1007/s11897-011-0062-8〉
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Soumis le : mercredi 18 juin 2014 - 14:24:04
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Magali Berthouze, Anne-Coline Laurent, Magali Breckler, Frank Lezoualc'H. New perspectives in cAMP-signaling modulation.. Curr Heart Fail Rep, 2011, 8 (3), pp.159-67. 〈10.1007/s11897-011-0062-8〉. 〈inserm-01009680〉



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