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European Heart Journal Advance Access originally published online on July 29, 2005
European Heart Journal 2005 26(17):1695-1696; doi:10.1093/eurheartj/ehi355
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© The European Society of Cardiology 2005. All rights reserved. For Permissions, please e-mail: journals.permissions@oupjournals.org

Lymphocyte GRK levels as biomarkers in heart failure

Stephen B. Liggett*

CardioPulmonary Research Center, University of Cincinnati College of Medicine, 231 Albert Sabin Way, Room G-062, Cincinnati, OH 45267-0564, USA

* Corresponding author. Tel: +1 513 558 0484; fax: +1 513 558 0835. E-mail address: stephen.liggett@uc.edu

This editorial refers to ‘Elevated myocardial and lymphocyte GRK2 expression and activity in human heart failure’{dagger} by G. Iaccarino et al., on page 1752

The first 10% of the full text of this article appears below.

Seven transmembrane (7-TM) receptors, also termed G-protein coupled receptors, represent one of the largest signalling families in the human genome. The ß1- and ß2-adrenergic receptors (ß1- and ß2ARs) are prototypic of many members of this family. In the classic paradigm, when occupied by agonist, both ßAR subtypes couple to the stimulatory G-protein Gs, whose {alpha} subunit activates adenylyl cyclase, increasing intracellular cAMP and activating protein kinase A (PKA), which phosphorylates multiple proteins in the heart leading to enhanced inotropy and chronotropy. This scenario, however, is not a simple, series-type switch. Instead, it can be viewed as a network consisting of switches, potentiometers, amplifiers, and attenuators in series and in parallel. Indeed, we now know that adrenergic receptors can couple to multiple G-proteins and can . . . [Full Text of this Article]


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Related articles in EHJ:

Elevated myocardial and lymphocyte GRK2 expression and activity in human heart failure
Guido Iaccarino, Emanuele Barbato, Ersilia Cipolletta, Vincenzo De Amicis, Kenneth B. Margulies, Dario Leosco, Bruno Trimarco, and Walter J. Koch
EHJ 2005 26: 1752-1758. [Abstract] [FREE Full Text]