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Effects of aldosterone on transient outward K+ current density in rat ventricular myocytesEpac enhances excitation-transcription coupling in cardiac myocytesSustained Epac activation induces calmodulin dependent positive inotropic effect in adult cardiomyocytesParadoxical effect of increased diastolic Ca(2+) release and decreased sinoatrial node activity in a mouse model of catecholaminergic polymorphic ventricular tachycardia.RyR2R420Q catecholaminergic polymorphic ventricular tachycardia mutation induces bradycardia by disturbing the coupled clock pacemaker mechanism.Increased Ca2+ sensitivity of the ryanodine receptor mutant RyR2R4496C underlies catecholaminergic polymorphic ventricular tachycardia.Abnormal Ca2+ spark/STOC coupling in cerebral artery smooth muscle cells of obese type 2 diabetic mice.Reconciling depressed Ca2+ sparks occurrence with enhanced RyR2 activity in failing mice cardiomyocytes.'Ca(2+)-induced Ca(2+) entry' or how the L-type Ca(2+) channel remodels its own signalling pathway in cardiac cells.Transient Receptor Potential Canonical (TRPC)/Orai1-dependent Store-operated Ca2+ Channels: NEW TARGETS OF ALDOSTERONE IN CARDIOMYOCYTES.Adjacent pore-lining residues within sodium channels identified by paired cysteine mutagenesis.L-type Ca(2+) current in ventricular cardiomyocytes.Epac in cardiac calcium signaling.Calcium signaling in diabetic cardiomyocytes.Direct and indirect effects of aldosterone on cyclooxygenase-2 and interleukin-6 expression in rat cardiac cells in culture and after myocardial infarction.Mineralocorticoid receptor antagonism prevents the electrical remodeling that precedes cellular hypertrophy after myocardial infarction.Mineralocorticoid modulation of cardiac ryanodine receptor activity is associated with downregulation of FK506-binding proteins.Conditional FKBP12.6 overexpression in mouse cardiac myocytes prevents triggered ventricular tachycardia through specific alterations in excitation-contraction coupling.Beneficial effects of leptin treatment in a setting of cardiac dysfunction induced by transverse aortic constriction in mouse.Proton inhibition of sodium channels: mechanism of gating shifts and reduced conductance.Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion.Cardiomyocyte Overexpression of Neuronal Nitric Oxide Synthase Delays Transition Toward Heart Failure in Response to Pressure Overload by Preserving Calcium CyclingCardioprotective action of urocortin in postconditioning involves recovery of intracellular calcium handlingThe cAMP binding protein Epac modulates Ca2+ sparks by a Ca2+/calmodulin kinase signalling pathway in rat cardiac myocytesHeterogeneity of the early outward current in ventricular cells isolated from normal and hypertrophied rat heartsConditional glucocorticoid receptor expression in the heart induces atrio-ventricular blockNeuropeptide Y rapidly enhances [Ca2+]i transients and Ca2+ sparks in adult rat ventricular myocytes through Y1 receptor and PLC activationProarrhythmic effect of sustained EPAC activation on TRPC3/4 in rat ventricular cardiomyocytesSpecific Activation of the Alternative Cardiac Promoter of Cacna1c by the Mineralocorticoid ReceptorProgression of excitation-contraction coupling defects in doxorubicin cardiotoxicityArrhythmias precede cardiomyopathy and remodeling of Ca2+ handling proteins in a novel model of long QT syndromeSpecific Upregulation of TRPC1 and TRPC5 Channels by Mineralocorticoid Pathway in Adult Rat Ventricular CardiomyocytesOrai1 Channel Inhibition Preserves Left Ventricular Systolic Function and Normal Ca2+ Handling After Pressure Overload
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P50
description
researcher
@en
wetenschapper
@nl
հետազոտող
@hy
name
Jean-Pierre Benitah
@ast
Jean-Pierre Benitah
@en
Jean-Pierre Benitah
@es
Jean-Pierre Benitah
@nl
type
label
Jean-Pierre Benitah
@ast
Jean-Pierre Benitah
@en
Jean-Pierre Benitah
@es
Jean-Pierre Benitah
@nl
prefLabel
Jean-Pierre Benitah
@ast
Jean-Pierre Benitah
@en
Jean-Pierre Benitah
@es
Jean-Pierre Benitah
@nl
P106
P21
P31
P496
0000-0002-9866-9081