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Review ArticleMINIREVIEW

Contributions of Protein Kinase A Anchoring Proteins to Compartmentation of cAMP Signaling in the Heart

Michael S. Kapiloff
Molecular Pharmacology August 2002, 62 (2) 193-199; DOI: https://doi.org/10.1124/mol.62.2.193
Michael S. Kapiloff
Department of Pediatrics, Heart Research Center, Oregon Health and Science University, Portland, Oregon
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Abstract

The cAMP-dependent protein kinase (PKA) transduces signals in the heart initiated by β1-adrenergic, G-protein-coupled receptors after norepinephrine, sympathetic stimulation. Signaling through this pathway results in a characteristic set of cellular responses, including increases in ion fluxes and contractile strength, mobilization of energy stores, and changes in gene expression. Not all receptors that activate adenylate cyclase and increase cAMP levels, however, cause the cardiac myocyte to react in this manner. Research in the field of signal transduction over the last 25 years has addressed this issue of specificity in signaling by diffusable second messengers. PKA is in part targeted to discrete cellular locations by A-kinase anchoring proteins. Through anchoring and formation of multienzyme complexes, specific, localized signal transduction is possible. I discuss in this review recent advances in the understanding of PKA signaling complexes in the cardiac myocyte.

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Molecular Pharmacology: 62 (2)
Molecular Pharmacology
Vol. 62, Issue 2
1 Aug 2002
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Review ArticleMINIREVIEW

Contributions of Protein Kinase A Anchoring Proteins to Compartmentation of cAMP Signaling in the Heart

Michael S. Kapiloff
Molecular Pharmacology August 1, 2002, 62 (2) 193-199; DOI: https://doi.org/10.1124/mol.62.2.193

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Review ArticleMINIREVIEW

Contributions of Protein Kinase A Anchoring Proteins to Compartmentation of cAMP Signaling in the Heart

Michael S. Kapiloff
Molecular Pharmacology August 1, 2002, 62 (2) 193-199; DOI: https://doi.org/10.1124/mol.62.2.193
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  • Article
    • Abstract
    • Evidence for Localized PKA Signaling
    • A-Kinase Anchoring Proteins
    • Cardiac AKAPs
    • AKAP 18/15 and the L-Type Ca2+ Channel
    • Yotiao and Long-QT Syndrome
    • mAKAP and the Ryanodine Receptor
    • Conclusions
    • Acknowledgments
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