High basal protein kinase A-dependent phosphorylation drives rhythmic internal Ca2+ store oscillations and spontaneous beating of cardiac pacemaker cells.
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Ectopic activity in the rat pulmonary vein can arise from simultaneous activation of alpha1- and beta1-adrenoceptorsGenome-wide association analysis identifies multiple loci related to resting heart rateMechanisms underlying the cardiac pacemaker: the role of SK4 calcium-activated potassium channelsIon Channels in the HeartModern concepts concerning the origin of the heartbeat.The importance of Ca(2+)-dependent mechanisms for the initiation of the heartbeatOverexpression of 14-3-3z promotes tau phosphorylation at Ser262 and accelerates proteosomal degradation of synaptophysin in rat primary hippocampal neuronsInotropy and L-type Ca2+ current, activated by beta1- and beta2-adrenoceptors, are differently controlled by phosphodiesterases 3 and 4 in rat heartUrocortin induces positive inotropic effect in rat heartDirect conversion of quiescent cardiomyocytes to pacemaker cells by expression of Tbx18.Hierarchical clustering of ryanodine receptors enables emergence of a calcium clock in sinoatrial node cells.Ca²⁺-dependent phosphorylation of Ca²⁺ cycling proteins generates robust rhythmic local Ca²⁺ releases in cardiac pacemaker cells.Inositol-1,4,5-trisphosphate-mediated spontaneous activity in mouse embryonic stem cell-derived cardiomyocytes.I(f) and SR Ca(2+) release both contribute to pacemaker activity in canine sinoatrial node cellsAge-associated abnormalities of intrinsic automaticity of sinoatrial nodal cells are linked to deficient cAMP-PKA-Ca(2+) signalingYin and yang of the cardiac pacemaker clock system in health and disease.A coupled SYSTEM of intracellular Ca2+ clocks and surface membrane voltage clocks controls the timekeeping mechanism of the heart's pacemaker.A paradigm shift for the heart's pacemaker.Synchronization of sinoatrial node pacemaker cell clocks and its autonomic modulation impart complexity to heart beating intervals.Computer algorithms for automated detection and analysis of local Ca2+ releases in spontaneously beating cardiac pacemaker cellsA novel quantitative explanation for the autonomic modulation of cardiac pacemaker cell automaticity via a dynamic system of sarcolemmal and intracellular proteins.Mechanisms of sinoatrial node dysfunction in a canine model of pacing-induced atrial fibrillation.Phosphorylation and modulation of hyperpolarization-activated HCN4 channels by protein kinase A in the mouse sinoatrial nodeSarcoplasmic reticulum Ca2+ pumping kinetics regulates timing of local Ca2+ releases and spontaneous beating rate of rabbit sinoatrial node pacemaker cells.Tachybradycardia in the isolated canine right atrium induced by chronic sympathetic stimulation and pacemaker current inhibition.Synergistic dual automaticity in sinoatrial node cell and tissue models.Crosstalk between mitochondrial and sarcoplasmic reticulum Ca2+ cycling modulates cardiac pacemaker cell automaticity.Rhythmic beating of stem cell-derived cardiac cells requires dynamic coupling of electrophysiology and Ca cycling.Synchronization of stochastic Ca²(+) release units creates a rhythmic Ca²(+) clock in cardiac pacemaker cellsCa²+/calmodulin-dependent protein kinase II (CaMKII) activity and sinoatrial nodal pacemaker cell energetics.The role of the calcium and the voltage clocks in sinoatrial node dysfunction.Catecholamine-independent heart rate increases require Ca2+/calmodulin-dependent protein kinase II.Complete atrial-specific knockout of sodium-calcium exchange eliminates sinoatrial node pacemaker activity.Myristoylated peptides potentiate the funny current (I(f)) in sinoatrial myocytes.Calcium and arrhythmogenesis.Store-operated calcium entry and the localization of STIM1 and Orai1 proteins in isolated mouse sinoatrial node cells.Dopamine-induced oscillations of the pyloric pacemaker neuron rely on release of calcium from intracellular storesCa2+-regulated-cAMP/PKA signaling in cardiac pacemaker cells links ATP supply to demand.A full range of mouse sinoatrial node AP firing rates requires protein kinase A-dependent calcium signaling.Heart Rate Acceleration of a Subsidiary Pacemaker by β-Adrenergic Stimulation.
P2860
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P2860
High basal protein kinase A-dependent phosphorylation drives rhythmic internal Ca2+ store oscillations and spontaneous beating of cardiac pacemaker cells.
description
2006 nî lūn-bûn
@nan
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
2006年论文
@zh
2006年论文
@zh-cn
name
High basal protein kinase A-de ...... ng of cardiac pacemaker cells.
@en
High basal protein kinase A-de ...... ng of cardiac pacemaker cells.
@nl
type
label
High basal protein kinase A-de ...... ng of cardiac pacemaker cells.
@en
High basal protein kinase A-de ...... ng of cardiac pacemaker cells.
@nl
prefLabel
High basal protein kinase A-de ...... ng of cardiac pacemaker cells.
@en
High basal protein kinase A-de ...... ng of cardiac pacemaker cells.
@nl
P2093
P50
P1433
P1476
High basal protein kinase A-de ...... ng of cardiac pacemaker cells.
@en
P2093
Abdul M Ruknudin
Dongmei Yang
Heping Cheng
James L Caffrey
Matthew Barlow
Michael D Stern
Rui-Ping Xiao
Shavsha Johnson
Shekhar Deo
Syevda Sirenko
P304
P356
10.1161/01.RES.0000204575.94040.D1
P577
2006-01-19T00:00:00Z