Conventional protein kinase C isoforms and cross-activation of protein kinase A regulate cardiac Na+ current

FEBS Letters
H G Shin, Katherine T Murray

Abstract

We tested the hypothesis that specific isoforms of protein kinase C (PKC) are responsible for modulation of Na+ current (I(Na)) derived from the human cardiac Na+ channel using activators and inhibitors selective for specific PKCs. Experimental results demonstrated that I(Na) suppression was mediated by activation of conventional PKCs (cPKCs) and possibly resulted from channel internalization. In the presence of cPKC inhibition, phorbol ester application unexpectedly increased Na+ current, an effect eliminated by inhibition of protein kinase A. These findings demonstrate complex modulation of cardiac I(Na) by protein kinases and provide further evidence that PKC isoforms have distinct protein targets.

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Citations

Feb 12, 2004·Journal of Molecular and Cellular Cardiology·Lucas J HerfstHabo J Jongsma
Sep 23, 2011·Cardiovascular Research·Martin B RookMarti F A Bierhuizen
Nov 22, 2011·American Journal of Physiology. Heart and Circulatory Physiology·Haifa HallaqKatherine T Murray
Sep 12, 2009·Circulation Research·Man LiuSamuel C Dudley
Mar 10, 2015·Journal of Molecular and Cellular Cardiology·Céline Marionneau, Hugues Abriel
Oct 8, 2011·Journal of Molecular and Cellular Cardiology·Euy-Myoung JeongSamuel C Dudley
Oct 27, 2018·Acta Physiologica·Shahid M Iqbal, Rosa Lemmens-Gruber
Jun 6, 2006·American Journal of Physiology. Heart and Circulatory Physiology·J GuoH J Duff
May 10, 2005·The Journal of Pharmacology and Experimental Therapeutics·Didi OmiyiLindon H Young

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