The LQT syndromes – current status of molecular mechanisms
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W. Haverkamp | G. Breithardt | M. Borggrefe | G. Breithardt | W. Haverkamp | M. Borggrefe | E. Schulze-Bahr | G. Assmann | H. Wedekind | H. Funke | E. Schulze-Bahr | H. Wedekind | G. Assmann | H. Funke | Martin Borggrefe
[1] J. Warmke,et al. HERG Sequence Correction , 1996, Science.
[2] Y. Mori,et al. A Cellular Model for Long QT Syndrome , 1997, The Journal of Biological Chemistry.
[3] A. Jervell,et al. The surdo-cardiac syndrome: three new cases of congenital deafness with syncopal attacks and Q-T prolongation in the electrocardiogram. , 1966, American heart journal.
[4] A. George,et al. Pharmacological targeting of long QT mutant sodium channels. , 1997, The Journal of clinical investigation.
[5] Craig T. January,et al. Early Afterdepolarizations: Mechanism of Induction and Block A Role for L‐Type Ca2+ Current , 1989, Circulation research.
[6] P. Coumel,et al. A novel mutation in the potassium channel gene KVLQT1 causes the Jervell and Lange-Nielsen cardioauditory syndrome , 1997, Nature Genetics.
[7] E. Green,et al. A molecular basis for cardiac arrhythmia: HERG mutations cause long QT syndrome , 1995, Cell.
[8] R. Kass,et al. Lidocaine block of LQT-3 mutant human Na+ channels. , 1996, Circulation research.
[9] Gary Yellen,et al. The inward rectification mechanism of the HERG cardiac potassium channel , 1996, Nature.
[10] J. Mason,et al. Genetically defined therapy of inherited long-QT syndrome. Correction of abnormal repolarization by potassium. , 1996, Circulation.
[11] M. Sanguinetti,et al. Spectrum of HERG K+-channel dysfunction in an inherited cardiac arrhythmia. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[12] J. Weissenbach,et al. Readjusting the localization of long QT syndrome gene on chromosome 11p15. , 1995, Comptes rendus de l'Academie des sciences. Serie III, Sciences de la vie.
[13] M. Jiang,et al. Suppression of Slow Delayed Rectifier Current by a Truncated Isoform of KvLQT1 Cloned from Normal Human Heart* , 1997, The Journal of Biological Chemistry.
[14] G. Breithardt,et al. KCNE1 mutations cause Jervell and Lange-Nielsen syndrome , 1997, Nature Genetics.
[15] A. Brown,et al. Molecular physiology and pharmacology of HERG. Single-channel currents and block by dofetilide. , 1996, Circulation.
[16] H. Morita,et al. Early Afterdepolarization Abolished by Potassium Channel Opener in a Patient with Idiopathic Long QT Syndrome , 1995, Journal of cardiovascular electrophysiology.
[17] M. Sanguinetti,et al. Mutations in the hminK gene cause long QT syndrome and suppress lKs function , 1997, Nature Genetics.
[18] P. Coumel,et al. Heterozygous mutation in the pore of potassium channel gene KvLQT1 causes an apparently normal phenotype in long QT syndrome , 1998, European Journal of Human Genetics.
[19] M J Ackerman,et al. The long QT syndrome: ion channel diseases of the heart. , 1998, Mayo Clinic proceedings.
[20] CharlesAntzelevitch,et al. Sodium Channel Block With Mexiletine Is Effective in Reducing Dispersion of Repolarization and Preventing Torsade de Pointes in LQT2 and LQT3 Models of the Long-QT Syndrome , 1997 .
[21] R. Matsuoka,et al. A de novo missense mutation of human cardiac Na+ channel exhibiting novel molecular mechanisms of long QT syndrome , 1998, FEBS letters.
[22] B. Kerem,et al. Novel LQT-3 Mutation Affects Na+ Channel Activity Through Interactions Between α- and β1-Subunits , 1998 .
[23] R Lazzara,et al. Multiple mechanisms in the long-QT syndrome. Current knowledge, gaps, and future directions. The SADS Foundation Task Force on LQTS. , 1996, Circulation.
[24] M. Blanar,et al. Dominant-negative KvLQT1 mutations underlie the LQT1 form of long QT syndrome. , 1997, Circulation.
[25] L. Carlsson,et al. Antiarrhythmic Effects of Potassium Channel Openers in Rhythm Abnormalities Related to Delayed Repolarization , 1992, Circulation.
[26] M. Blanar,et al. KvLQT1, a voltage-gated potassium channel responsible for human cardiac arrhythmias. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[27] M. Leppert,et al. Locus heterogeneity of autosomal dominant long QT syndrome. , 1993, The Journal of clinical investigation.
[28] M. Keating,et al. Molecular basis of the long-QT syndrome associated with deafness. , 1997, The New England journal of medicine.
[29] A. George,et al. Characterization of human cardiac Na+ channel mutations in the congenital long QT syndrome. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[30] M. Sanguinetti,et al. Class III antiarrhythmic drugs block HERG, a human cardiac delayed rectifier K+ channel. Open-channel block by methanesulfonanilides. , 1996, Circulation research.
[31] G. Robertson,et al. HERG, a human inward rectifier in the voltage-gated potassium channel family. , 1995, Science.
[32] A. Brown,et al. Cloned human inward rectifier K+ channel as a target for class III methanesulfonanilides. , 1995, Circulation research.
[33] A. Wilde,et al. A Dominant Negative Isoform of the Long QT Syndrome 1 Gene Product* , 1998, The Journal of Biological Chemistry.
[34] Jacques Barhanin,et al. KvLQT1 and IsK (minK) proteins associate to form the IKS cardiac potassium current , 1996, Nature.
[35] G. Breithardt,et al. Autosomal recessive long-QT syndrome (Jervell Lange-Nielsen syndrome) is genetically heterogeneous , 1997, Human Genetics.
[36] M. Leppert,et al. The spectrum of symptoms and QT intervals in carriers of the gene for the long-QT syndrome. , 1992, The New England journal of medicine.
[37] H. Tan,et al. Electrophysiologic Mechanisms of the Long QT Interval Syndromes and Torsade de Pointes , 1995, Annals of Internal Medicine.
[38] M. Sanguinetti,et al. Fast inactivation causes rectification of the IKr channel , 1996, The Journal of general physiology.
[39] M. Sanguinetti,et al. Coassembly of K(V)LQT1 and minK (IsK) proteins to form cardiac I(Ks) potassium channel. , 1996, Nature.
[40] S. Priori,et al. Long QT syndrome patients with mutations of the SCN5A and HERG genes have differential responses to Na+ channel blockade and to increases in heart rate. Implications for gene-specific therapy. , 1995, Circulation.
[41] G. Landes,et al. Positional cloning of a novel potassium channel gene: KVLQT1 mutations cause cardiac arrhythmias , 1996, Nature Genetics.
[42] Arthur J Moss,et al. SCN5A mutations associated with an inherited cardiac arrhythmia, long QT syndrome , 1995, Cell.
[43] P. Coumel,et al. A mutation in HERG associated with notched T waves in long QT syndrome. , 1996, Journal of molecular and cellular cardiology.
[44] 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.
[45] P. Coumel,et al. KVLQT1 C-terminal missense mutation causes a forme fruste long-QT syndrome. , 1997, Circulation.
[46] 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.
[47] J. Towbin,et al. Improvement of repolarization abnormalities by a K+ channel opener in the LQT1 form of congenital long-QT syndrome. , 1998, Circulation.
[48] S. Priori,et al. Cardiac sodium channel mutations in patients with long QT syndrome, an inherited cardiac arrhythmia. , 1995, Human molecular genetics.
[49] E. Mathews,et al. Q-T prolongation and ventricular arrhythmias, with and without deafness, in the same family. , 1972, The American journal of cardiology.
[50] P. Schwartz,et al. Multiple mechanisms of Na+ channel--linked long-QT syndrome. , 1996, Circulation research.
[51] M. Leppert,et al. Linkage of a cardiac arrhythmia, the long QT syndrome, and the Harvey ras-1 gene. , 1991, Science.
[52] J. Balser,et al. Phenotypic characterization of a novel long-QT syndrome mutation (R1623Q) in the cardiac sodium channel. , 1998, Circulation.
[53] M. Leppert,et al. Consistent linkage of the long-QT syndrome to the Harvey ras-1 locus on chromosome 11. , 1991, American journal of human genetics.
[54] A. George,et al. Molecular mechanism for an inherited cardiac arrhythmia , 1995, Nature.
[55] A. Moss,et al. ECG T-wave patterns in genetically distinct forms of the hereditary long QT syndrome. , 1995, Circulation.
[56] S. Priori,et al. The long QT syndrome. , 1997, Current problems in cardiology.
[57] S. Priori,et al. Differential response to Na+ channel blockade, beta-adrenergic stimulation, and rapid pacing in a cellular model mimicking the SCN5A and HERG defects present in the long-QT syndrome. , 1996, Circulation research.
[58] P Coumel,et al. Exclusion of KCNE1 (IsK) as a candidate gene for Jervell and Lange-Nielsen syndrome. , 1996, Journal of molecular and cellular cardiology.
[59] S. Priori,et al. A recessive variant of the Romano-Ward long-QT syndrome? , 1998, Circulation.
[60] B Attali,et al. Molecular Mechanism and Functional Significance of the MinK Control of the KvLQT1 Channel Activity* , 1997, The Journal of Biological Chemistry.
[61] B. Wollnik,et al. Pathophysiological Mechanisms of Dominant and Recessive Kvlqt1 K + Channel Mutations Found in Inherited Cardiac Arrhythmias , 1997 .
[62] 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.
[63] M. Sanguinetti,et al. A mechanistic link between an inherited and an acquird cardiac arrthytmia: HERG encodes the IKr potassium channel , 1995, Cell.
[64] D. Roden,et al. Incidence and clinical features of the quinidine-associated long QT syndrome: implications for patient care. , 1986, American heart journal.
[65] F. Charpentier,et al. Mapping of a gene for long QT syndrome to chromosome 4q25-27. , 1995, American journal of human genetics.
[66] M. Sanguinetti,et al. Coassembly of KVLQT1 and minK (IsK) proteins to form cardiac IKS potassium channel , 1996, Nature.