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Epac2-Rap1 Signaling Regulates Reactive Oxygen Species Production and Susceptibility to Cardiac Arrhythmias
Author(s) -
Zhaokang Yang,
Hannah M. Kirton,
Moza M. AlOwais,
Jérôme Thireau,
Sylvain Richard,
Chris Peers,
Derek S. Steele
Publication year - 2016
Publication title -
antioxidants and redox signaling
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.277
H-Index - 190
eISSN - 1557-7716
pISSN - 1523-0864
DOI - 10.1089/ars.2015.6485
Subject(s) - guanine nucleotide exchange factor , rap1 , microbiology and biotechnology , signal transduction , mitochondrial ros , reactive oxygen species , chemistry , pharmacology , biology
In the heart, β 1 -adrenergic signaling involves cyclic adenosine monophosphate (cAMP) acting via both protein kinase-A (PKA) and exchange protein directly activated by cAMP (Epac): a guanine nucleotide exchange factor for the small GTPase Rap1. Inhibition of Epac-Rap1 signaling has been proposed as a therapeutic strategy for both cancer and cardiovascular disease. However, previous work suggests that impaired Rap1 signaling may have detrimental effects on cardiac function. The aim of the present study was to investigate the influence of Epac2-Rap1 signaling on the heart using both in vivo and in vitro approaches.

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