SK channels and ventricular arrhythmias in heart failure.

[1]  P. Binkley,et al.  Calcium-Activated Potassium Current Modulates Ventricular Repolarization in Chronic Heart Failure , 2014, PloS one.

[2]  J. Weiss,et al.  Erratum: Apamin does not inhibit human cardiac Na+ current, L-type Ca2+ current or other major K+ currents (PLoS ONE (2014) 9, 5 (e96691) DOI: 10.1371/journal.pone.0096691) , 2014 .

[3]  J. Weiss,et al.  Apamin Does Not Inhibit Human Cardiac Na+ Current, L-type Ca2+ Current or Other Major K+ Currents , 2014, PloS one.

[4]  D. Terentyev,et al.  Sarcoplasmic reticulum Ca²⁺ release is both necessary and sufficient for SK channel activation in ventricular myocytes. , 2014, American journal of physiology. Heart and circulatory physiology.

[5]  Robert W. Mills,et al.  Overexpression of KCNN3 results in sudden cardiac death. , 2014, Cardiovascular research.

[6]  J. Weiss,et al.  Apamin induces early afterdepolarizations and torsades de pointes ventricular arrhythmia from failing rabbit ventricles exhibiting secondary rises in intracellular calcium. , 2013, Heart rhythm.

[7]  J. Weiss,et al.  Apamin‐Sensitive Calcium‐Activated Potassium Currents in Rabbit Ventricles with Chronic Myocardial Infarction , 2013, Journal of cardiovascular electrophysiology.

[8]  A. Ma,et al.  Bisoprolol reversed small conductance calcium-activated potassium channel (SK) remodeling in a volume-overload rat model , 2013, Molecular and Cellular Biochemistry.

[9]  Peng-Sheng Chen,et al.  Amiodarone Inhibits Apamin-Sensitive Potassium Currents , 2013, PloS one.

[10]  M. Fishbein,et al.  Low-level vagus nerve stimulation upregulates small conductance calcium-activated potassium channels in the stellate ganglion. , 2013, Heart rhythm.

[11]  J. Weiss,et al.  Apamin-Sensitive Potassium Current Modulates Action Potential Duration Restitution and Arrhythmogenesis of Failing Rabbit Ventricles , 2013, Circulation. Arrhythmia and electrophysiology.

[12]  A. Gadicherla,et al.  Protection against cardiac injury by small Ca(2+)-sensitive K(+) channels identified in guinea pig cardiac inner mitochondrial membrane. , 2013, Biochimica et biophysica acta.

[13]  B. Nguyen,et al.  Heterogeneous Upregulation of Apamin‐Sensitive Potassium Currents in Failing Human Ventricles , 2013, Journal of the American Heart Association.

[14]  Po-Cheng Chang,et al.  Proarrhythmic effect of blocking the small conductance calcium activated potassium channel in isolated canine left atrium. , 2012, Heart rhythm.

[15]  K. Lunetta,et al.  Meta-analysis identifies six new susceptibility loci for atrial fibrillation , 2012, Nature Genetics.

[16]  P. Sah,et al.  Small-conductance Ca2+-activated K+ channels: form and function. , 2012, Annual review of physiology.

[17]  John Dempster,et al.  Remodelling of human atrial K+ currents but not ion channel expression by chronic β-blockade , 2011, Pflügers Archiv - European Journal of Physiology.

[18]  M. Fishbein,et al.  Continuous Low-Level Vagus Nerve Stimulation Reduces Stellate Ganglion Nerve Activity and Paroxysmal Atrial Tachyarrhythmias in Ambulatory Canines , 2011, Circulation.

[19]  J. Weiss,et al.  Small-Conductance Calcium-Activated Potassium Channel and Recurrent Ventricular Fibrillation in Failing Rabbit Ventricles , 2011, Circulation research.

[20]  U. Sørensen,et al.  Inhibition of Small-Conductance Ca2+-Activated K+ Channels Terminates and Protects Against Atrial Fibrillation , 2010, Circulation. Arrhythmia and electrophysiology.

[21]  D. Jane,et al.  Small conductance calcium-activated potassium channels: From structure to function , 2010, Progress in Neurobiology.

[22]  Thomas Meitinger,et al.  Common Variants in KCNN3 are Associated with Lone Atrial Fibrillation , 2010, Nature Genetics.

[23]  Takeshi Aiba,et al.  Electrical remodeling in the failing heart , 2010, Current opinion in cardiology.

[24]  J. Valentin,et al.  An introduction to QT interval prolongation and non‐clinical approaches to assessing and reducing risk , 2010, British journal of pharmacology.

[25]  J. Papp,et al.  Does small-conductance calcium-activated potassium channel contribute to cardiac repolarization? , 2009, Journal of molecular and cellular cardiology.

[26]  J. Weiss,et al.  Mechanisms of recurrent ventricular fibrillation in a rabbit model of pacing-induced heart failure. , 2009, Heart rhythm.

[27]  Robert H. Anderson,et al.  Molecular Architecture of the Human Sinus Node: Insights Into the Function of the Cardiac Pacemaker , 2009, Circulation.

[28]  Zhao Zhang,et al.  Ablation of a Ca2+‐activated K+ channel (SK2 channel) results in action potential prolongation in atrial myocytes and atrial fibrillation , 2009, The Journal of physiology.

[29]  K. Thor,et al.  A Positive Modulator of KCa2 and KCa3 Channels, 4,5-Dichloro-1,3-diethyl-1,3-dihydro-benzoimidazol-2-one (NS4591), Inhibits Bladder Afferent Firing in Vitro and Bladder Overactivity in Vivo , 2009, Journal of Pharmacology and Experimental Therapeutics.

[30]  David W. Litchfield,et al.  Neurotransmitter Modulation of Small-Conductance Ca2+-Activated K+ Channels by Regulation of Ca2+ Gating , 2008, Neuron.

[31]  J. Adelman,et al.  Functional Roles of a Ca2+-Activated K+ Channel in Atrioventricular Nodes , 2008, Circulation research.

[32]  Masanori Hirose,et al.  Early electrical remodeling in rabbit pulmonary vein results from trafficking of intracellular SK2 channels to membrane sites. , 2007, Cardiovascular research.

[33]  Ling Lu,et al.  Molecular Coupling of a Ca2+-Activated K+ Channel to L-Type Ca2+ Channels via α-Actinin2 , 2007 .

[34]  Ling Lu,et al.  Differential expression of small-conductance Ca2+-activated K+ channels SK1, SK2, and SK3 in mouse atrial and ventricular myocytes. , 2005, American journal of physiology. Heart and circulatory physiology.

[35]  Yi Zhang,et al.  Molecular Identification and Functional Roles of a Ca2+-activated K+ Channel in Human and Mouse Hearts* , 2003, Journal of Biological Chemistry.

[36]  Charles Antzelevitch,et al.  Reinduction of Atrial Fibrillation Immediately After Termination of the Arrhythmia Is Mediated by Late Phase 3 Early Afterdepolarization–Induced Triggered Activity , 2003, Circulation.

[37]  J. Joseph,et al.  Tamapin, a Venom Peptide from the Indian Red Scorpion (Mesobuthus tamulus) That Targets Small Conductance Ca2+-activated K+ Channels and Afterhyperpolarization Currents in Central Neurons* , 2002, The Journal of Biological Chemistry.

[38]  S. Ro,et al.  Molecular properties of small-conductance Ca2+-activated K+ channels expressed in murine colonic smooth muscle. , 2001, American journal of physiology. Gastrointestinal and liver physiology.

[39]  N. Marrion,et al.  Small-Conductance, Calcium-Activated Potassium Channels from Mammalian Brain , 1996, Science.

[40]  W. Giles,et al.  Comparison of potassium currents in rabbit atrial and ventricular cells. , 1988, The Journal of physiology.

[41]  A. Feher,et al.  CALL FOR PAPERS Cardiovascular and Cerebrovascular Aging-New Mechanisms and Insights Age-related impairment of conducted dilation in human coronary arterioles , 2014 .

[42]  Qing-Hui Chen,et al.  Ventricular tachyarrhythmias in rats with acute myocardial infarction involves activation of small-conductance Ca2+-activated K+ channels. , 2013, American journal of physiology. Heart and circulatory physiology.

[43]  Ling Lu,et al.  Molecular coupling of a Ca2+-activated K+ channel to L-type Ca2+ channels via alpha-actinin2. , 2007, Circulation research.

[44]  Mark J. Miller,et al.  Selective blockers and manipulated channel expression levels , 2001 .