KCNE2 confers background current characteristics to the cardiac KCNQ1 potassium channel
暂无分享,去创建一个
[1] M. Sanguinetti. Maximal function of minimal K+ channel subunits. , 2000, Trends in pharmacological sciences.
[2] J. Barhanin,et al. Novel mutations in KvLQT1 that affect Iks activation through interactions with Isk. , 2000, Cardiovascular research.
[3] M. Chahine,et al. SCN5A mutation (T1620M) causing Brugada syndrome exhibits different phenotypes when expressed in Xenopus oocytes and mammalian cells , 2000, FEBS letters.
[4] S. Waldegger,et al. A constitutively open potassium channel formed by KCNQ1 and KCNE3 , 2000, Nature.
[5] M. Sanguinetti,et al. Long QT Syndrome-associated Mutations in the S4-S5 Linker of KvLQT1 Potassium Channels Modify Gating and Interaction with minK Subunits* , 1999, The Journal of Biological Chemistry.
[6] M. Sanguinetti,et al. Functional Effects of Mutations in KvLQT1 that Cause Long QT Syndrome , 1999, Journal of cardiovascular electrophysiology.
[7] M. Keating,et al. MiRP1 Forms IKr Potassium Channels with HERG and Is Associated with Cardiac Arrhythmia , 1999, Cell.
[8] R. Hauer,et al. Genetic and Molecular Basis of Cardiac Arrhythmias: Impact on Clinical Management , 2022 .
[9] M. Lazdunski,et al. Involvement of IsK-associated K+ channel in heart rate control of repolarization in a murine engineered model of Jervell and Lange-Nielsen syndrome. , 1998, Circulation research.
[10] M. Lazdunski,et al. IKs, a slow and intriguing cardiac K+ channel and its associated long QT diseases. , 1998, Trends in cardiovascular medicine.
[11] M. Lazdunski,et al. A neuronal two P domain K+ channel stimulated by arachidonic acid and polyunsaturated fatty acids , 1998, The EMBO journal.
[12] D. Roden. Taking the “Idio” out of “Idiosyncratic”: Predicting Torsades de Pointes , 1998, Pacing and clinical electrophysiology : PACE.
[13] A. Wilde,et al. A Dominant Negative Isoform of the Long QT Syndrome 1 Gene Product* , 1998, The Journal of Biological Chemistry.
[14] Priya D. Duggal,et al. Mutation of the gene for IsK associated with both Jervell and Lange-Nielsen and Romano-Ward forms of Long-QT syndrome. , 1998, Circulation.
[15] G. Breithardt,et al. KCNE1 mutations cause Jervell and Lange-Nielsen syndrome , 1997, Nature Genetics.
[16] M. Sanguinetti,et al. Mutations in the hminK gene cause long QT syndrome and suppress lKs function , 1997, Nature Genetics.
[17] M. Pembrey,et al. IsK and KvLQT1: mutation in either of the two subunits of the slow component of the delayed rectifier potassium channel can cause Jervell and Lange-Nielsen syndrome. , 1997, Human molecular genetics.
[18] B. Wollnik,et al. Pathophysiological Mechanisms of Dominant and Recessive Kvlqt1 K + Channel Mutations Found in Inherited Cardiac Arrhythmias , 1997 .
[19] M. Lazdunski,et al. Properties of KvLQT1 K+ channel mutations in Romano–Ward and Jervell and Lange‐Nielsen inherited cardiac arrhythmias , 1997, The EMBO journal.
[20] W. Stühmer,et al. The role of the IsK protein in the specific pharmacological properties of the IKs channel complex , 1997, British journal of pharmacology.
[21] P. Coumel,et al. A novel mutation in the potassium channel gene KVLQT1 causes the Jervell and Lange-Nielsen cardioauditory syndrome , 1997, Nature Genetics.
[22] M. Sanguinetti,et al. Coassembly of KVLQT1 and minK (IsK) proteins to form cardiac IKS potassium channel , 1996, Nature.
[23] Jacques Barhanin,et al. KvLQT1 and IsK (minK) proteins associate to form the IKS cardiac potassium current , 1996, Nature.
[24] B. Attali. A new wave for heart rhythms , 1996, Nature.
[25] B. Attali. Ion channels. A new wave for heart rhythms. , 1996, Nature.
[26] G. Landes,et al. Positional cloning of a novel potassium channel gene: KVLQT1 mutations cause cardiac arrhythmias , 1996, Nature Genetics.
[27] M. Sanguinetti,et al. Two components of cardiac delayed rectifier K+ current. Differential sensitivity to block by class III antiarrhythmic agents , 1990, The Journal of general physiology.
[28] S. Nakanishi,et al. Cloning of a membrane protein that induces a slow voltage-gated potassium current. , 1988, Science.
[29] A. Jervell,et al. CONGENITAL DEAF‐MUTISM, FUNCTIONAL HEART DISEASE WITH PROLONGATION OF THE Q‐T INTERVAL, AND SUDDEN DEATH , 1999, American heart journal.
[30] A. Jervell,et al. Congenital deaf-mutism, functional heart disease with prolongation of the Q-T interval, and sudden death , 1957 .