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Summary Anatomy Item Literature (2432) Expression Attributions Wiki
XB-ANAT-63

Papers associated with heart (and kcne1)

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Novel gene hKCNE4 slows the activation of the KCNQ1 channel., Teng S., Biochem Biophys Res Commun. April 11, 2003; 303 (3): 808-13.


Regulation of KCNE1-dependent K(+) current by the serum and glucocorticoid-inducible kinase (SGK) isoforms., Embark HM., Pflugers Arch. February 1, 2003; 445 (5): 601-6.


Inhibitory effect of the class III antiarrhythmic drug nifekalant on HERG channels: mode of action., Kushida S., Eur J Pharmacol. December 13, 2002; 457 (1): 19-27.


KCNE5 induces time- and voltage-dependent modulation of the KCNQ1 current., Angelo K., Biophys J. October 1, 2002; 83 (4): 1997-2006.


Inhibitory effects of volatile anesthetics on currents produced on heterologous expression of KvLQT1 and minK in Xenopus oocytes., Chen X., Vascul Pharmacol. July 1, 2002; 39 (1-2): 33-8.


A truncated splice variant of KCNQ1 cloned from rat heart., Yamada Y., Biochem Biophys Res Commun. June 7, 2002; 294 (2): 199-204.


Inhibition of cardiac potassium currents by pentobarbital., Bachmann A., Naunyn Schmiedebergs Arch Pharmacol. January 1, 2002; 365 (1): 29-37.


Dependence of I(Ks) biophysical properties on the expression system., Seebohm G., Pflugers Arch. September 1, 2001; 442 (6): 891-5.


MinK-related peptide 1: A beta subunit for the HCN ion channel subunit family enhances expression and speeds activation., Yu H., Circ Res. June 22, 2001; 88 (12): E84-7.


Chromanol 293B, a blocker of the slow delayed rectifier K+ current (IKs), inhibits the CFTR Cl- current., Bachmann A., Naunyn Schmiedebergs Arch Pharmacol. June 1, 2001; 363 (6): 590-6.


minK-related peptide 1 associates with Kv4.2 and modulates its gating function: potential role as beta subunit of cardiac transient outward channel?, Zhang M., Circ Res. May 25, 2001; 88 (10): 1012-9.


Identification of specific pore residues mediating KCNQ1 inactivation. A novel mechanism for long QT syndrome., Seebohm G., J Biol Chem. April 27, 2001; 276 (17): 13600-5.


Blocking effects of the antiarrhythmic drug propafenone on the HERG potassium channel., Mergenthaler J., Naunyn Schmiedebergs Arch Pharmacol. April 1, 2001; 363 (4): 472-80.


Short- and long-term effects of amiodarone on the two components of cardiac delayed rectifier K(+) current., Kamiya K., Circulation. March 6, 2001; 103 (9): 1317-24.


Inhibition of IKs channels by HMR 1556., Gögelein H., Naunyn Schmiedebergs Arch Pharmacol. December 1, 2000; 362 (6): 480-8.


Functional coupling of human beta 3-adrenoreceptors to the KvLQT1/MinK potassium channel., Kathöfer S., J Biol Chem. September 1, 2000; 275 (35): 26743-7.


Molecular basis for differential sensitivity of KCNQ and I(Ks) channels to the cognitive enhancer XE991., Wang HS., Mol Pharmacol. June 1, 2000; 57 (6): 1218-23.


Norpropoxyphene-induced cardiotoxicity is associated with changes in ion-selectivity and gating of HERG currents., Ulens C., Cardiovasc Res. December 1, 1999; 44 (3): 568-78.


Sensitivity of the slow component of the delayed rectifier potassium current (IKs) to potassium channel blockers: implications for clinical reverse use-dependent effects., Lai L., J Biomed Sci. January 1, 1999; 6 (4): 251-9.


Molecular and functional characterization of s-KCNQ1 potassium channel from rectal gland of Squalus acanthias., Waldegger S., Pflugers Arch. January 1, 1999; 437 (2): 298-304.


Independent and exclusive modulation of cardiac delayed rectifying K+ current by protein kinase C and protein kinase A., Lo CF., Circ Res. November 16, 1998; 83 (10): 995-1002.


Activation and inactivation of homomeric KvLQT1 potassium channels., Pusch M., Biophys J. August 1, 1998; 75 (2): 785-92.


A novel benzodiazepine that activates cardiac slow delayed rectifier K+ currents., Salata JJ., Mol Pharmacol. July 1, 1998; 54 (1): 220-30.


Effects of the chromanol 293B, a selective blocker of the slow, component of the delayed rectifier K+ current, on repolarization in human and guinea pig ventricular myocytes., Bosch RF., Cardiovasc Res. May 1, 1998; 38 (2): 441-50.


Gating of I(sK) channels expressed in Xenopus oocytes., Tzounopoulos T., Biophys J. May 1, 1998; 74 (5): 2299-305.


The conduction pore of a cardiac potassium channel., Tai KK., Nature. February 5, 1998; 391 (6667): 605-8.


Blockade of HERG channels by the class III antiarrhythmic azimilide: mode of action., Busch AE., Br J Pharmacol. January 1, 1998; 123 (1): 23-30.


Suppression of slow delayed rectifier current by a truncated isoform of KvLQT1 cloned from normal human heart., Jiang M., J Biol Chem. September 26, 1997; 272 (39): 24109-12.


The role of the IsK protein in the specific pharmacological properties of the IKs channel complex., Busch AE., Br J Pharmacol. September 1, 1997; 122 (2): 187-9.


Block by propofol and thiopentone of the min K current (IsK) expressed in Xenopus oocytes., Heath BM., Naunyn Schmiedebergs Arch Pharmacol. September 1, 1997; 356 (3): 404-9.


KVLQT channels are inhibited by the K+ channel blocker 293B., Bleich M., Pflugers Arch. August 1, 1997; 434 (4): 499-501.


A minK-HERG complex regulates the cardiac potassium current I(Kr)., McDonald TV., Nature. July 17, 1997; 388 (6639): 289-92.


Properties and regulation of the minK potassium channel protein., Kaczmarek LK., Physiol Rev. July 1, 1997; 77 (3): 627-41.


KvLQT1, a voltage-gated potassium channel responsible for human cardiac arrhythmias., Yang WP., Proc Natl Acad Sci U S A. April 15, 1997; 94 (8): 4017-21.


MinK potassium channels are heteromultimeric complexes., Tai KK., J Biol Chem. January 17, 1997; 272 (3): 1654-8.


I(sK) Channel in Strial Marginal Cells. Voltage-Dependence, Ion-Selectivity, Inhibition by 293B and Sensitivity to Clofilium., Shen Z., Audit Neurosci. January 1, 1997; 3 (3): 215-230.


IK of rabbit ventricle is composed of two currents: evidence for IKs., Salata JJ., Am J Physiol. December 1, 1996; 271 (6 Pt 2): H2477-89.


Coassembly of K(V)LQT1 and minK (IsK) proteins to form cardiac I(Ks) potassium channel., Sanguinetti MC., Nature. November 7, 1996; 384 (6604): 80-3.


Inhibition of IKs in guinea pig cardiac myocytes and guinea pig IsK channels by the chromanol 293B., Busch AE., Pflugers Arch. October 1, 1996; 432 (6): 1094-6.


Effect of channel modulation and pH on IsK inhibition by the novel class III antiarrhythmic azimilide (NE-10064)., Herzer T., Eur J Pharmacol. October 15, 1995; 291 (2): 205-8.


A corticosteroid-induced gene expressing an "IsK-like" K+ channel activity in Xenopus oocytes., Attali B., Proc Natl Acad Sci U S A. June 20, 1995; 92 (13): 6092-6.


Differential expression of Isk mRNAs in mouse tissue during development and pregnancy., Felipe A., Am J Physiol. September 1, 1994; 267 (3 Pt 1): C700-5.


The novel class III antiarrhythmics NE-10064 and NE-10133 inhibit IsK channels expressed in Xenopus oocytes and IKs in guinea pig cardiac myocytes., Busch AE., Biochem Biophys Res Commun. July 15, 1994; 202 (1): 265-70.


K+ currents expressed from the guinea pig cardiac IsK protein are enhanced by activators of protein kinase C., Zhang ZJ., Proc Natl Acad Sci U S A. March 1, 1994; 91 (5): 1766-70.


The min K channel underlies the cardiac potassium current IKs and mediates species-specific responses to protein kinase C., Varnum MD., Proc Natl Acad Sci U S A. December 15, 1993; 90 (24): 11528-32.


Effects of [Ca2+]i and temperature on minK channels expressed in Xenopus oocytes., Busch AE., FEBS Lett. November 15, 1993; 334 (2): 221-4.


Expression of a minimal K+ channel protein in mammalian cells and immunolocalization in guinea pig heart., Freeman LC., Circ Res. November 1, 1993; 73 (5): 968-73.


The protein IsK is a dual activator of K+ and Cl- channels., Attali B., Nature. October 28, 1993; 365 (6449): 850-2.


Receptor-mediated regulation of IsK, a very slowly activating, voltage-dependent K+ channel in Xenopus oocytes., Honore E., Biochem Biophys Res Commun. May 15, 1992; 184 (3): 1135-41.


ISK, a slowly activating voltage-sensitive K+ channel. Characterization of multiple cDNAs and gene organization in the mouse., Lesage F., FEBS Lett. April 20, 1992; 301 (2): 168-72.

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