Identification of a targeted and testable antiarrhythmic therapy for long-QT syndrome type 2 using a patient-specific cellular model
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P. Schwartz | M. Mura | A. Mehta | C. Ramachandra | L. Crotti | W. Shim | M. Gnecchi | P. Wong | Pritpal Singh | Anuja Chitre | C. B. Lua | Chong Hui Lua
[1] P. Schwartz,et al. The KCNH2-IVS9-28A/G mutation causes aberrant isoform expression and hERG trafficking defect in cardiomyocytes derived from patients affected by Long QT Syndrome type 2. , 2017, International journal of cardiology.
[2] M. Mura,et al. Induced pluripotent stem cell technology: Toward the future of cardiac arrhythmias. , 2017, International journal of cardiology.
[3] Stefano Severi,et al. Elucidating arrhythmogenic mechanisms of long-QT syndrome CALM1-F142L mutation in patient-specific induced pluripotent stem cell-derived cardiomyocytes , 2017, Cardiovascular research.
[4] E. Deeks. Lumacaftor/Ivacaftor: A Review in Cystic Fibrosis , 2016, Drugs.
[5] M. Ackerman,et al. Calcium Revisited: New Insights Into the Molecular Basis of Long-QT Syndrome. , 2016, Circulation. Arrhythmia and electrophysiology.
[6] M. Zaccolo,et al. Correctors of mutant CFTR enhance subcortical cAMP–PKA signaling through modulating ezrin phosphorylation and cytoskeleton organization , 2016, Journal of Cell Science.
[7] C. January,et al. Molecular pathogenesis of long QT syndrome type 2 , 2016, Journal of arrhythmia.
[8] Andrea Mazzanti,et al. [2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death]. , 2015, Kardiologia polska.
[9] A. Karma,et al. Hyperphosphorylation of RyRs Underlies Triggered Activity in Transgenic Rabbit Model of LQT2 Syndrome , 2014, Circulation research.
[10] A. Mehta,et al. Phasic modulation of Wnt signaling enhances cardiac differentiation in human pluripotent stem cells by recapitulating developmental ontogeny. , 2014, Biochimica et biophysica acta.
[11] P. Schwartz. Cardiac sympathetic denervation to prevent life-threatening arrhythmias , 2014, Nature Reviews Cardiology.
[12] A. Mehta,et al. Re-trafficking of hERG reverses long QT syndrome 2 phenotype in human iPS-derived cardiomyocytes. , 2014, Cardiovascular research.
[13] Michael J Ackerman,et al. The long QT syndrome: a transatlantic clinical approach to diagnosis and therapy. , 2013, European heart journal.
[14] Susan S. Taylor,et al. Integrins protect cardiomyocytes from ischemia/reperfusion injury. , 2013, The Journal of clinical investigation.
[15] Michael J Ackerman,et al. Impact of genetics on the clinical management of channelopathies. , 2013, Journal of the American College of Cardiology.
[16] M. Kohlhaas,et al. Calcium release microdomains and mitochondria. , 2013, Cardiovascular research.
[17] Philip Wong,et al. Pharmacoelectrophysiology of viral-free induced pluripotent stem cell-derived human cardiomyocytes. , 2013, Toxicological sciences : an official journal of the Society of Toxicology.
[18] Lia Crotti,et al. Long-QT syndrome: from genetics to management. , 2012, Circulation. Arrhythmia and electrophysiology.
[19] P. Negulescu,et al. Correction of the F508del-CFTR protein processing defect in vitro by the investigational drug VX-809 , 2011, Proceedings of the National Academy of Sciences.
[20] J. Clancy,et al. Results of a phase IIa study of VX-809, an investigational CFTR corrector compound, in subjects with cystic fibrosis homozygous for the F508del-CFTR mutation , 2011, Thorax.
[21] Karl-Ludwig Laugwitz,et al. Patient-specific induced pluripotent stem-cell models for long-QT syndrome. , 2010, The New England journal of medicine.
[22] L. Jordaens,et al. Who Are the Long-QT Syndrome Patients Who Receive an Implantable Cardioverter-Defibrillator and What Happens to Them?: Data From the European Long-QT Syndrome Implantable Cardioverter-Defibrillator (LQTS ICD) Registry , 2010, Circulation.
[23] B. Horne,et al. Nonsense Mutations in hERG Cause a Decrease in Mutant mRNA Transcripts by Nonsense-Mediated mRNA Decay in Human Long-QT Syndrome , 2007, Circulation.
[24] D. Bers,et al. Ca2+/Calmodulin–Dependent Protein Kinase Modulates Cardiac Ryanodine Receptor Phosphorylation and Sarcoplasmic Reticulum Ca2+ Leak in Heart Failure , 2005, Circulation research.
[25] S. Reiken,et al. Enhancing calstabin binding to ryanodine receptors improves cardiac and skeletal muscle function in heart failure. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[26] Calum A MacRae,et al. Risk stratification in the long-QT syndrome. , 2003, The New England journal of medicine.
[27] D. Burkhoff,et al. PKA Phosphorylation Dissociates FKBP12.6 from the Calcium Release Channel (Ryanodine Receptor) Defective Regulation in Failing Hearts , 2000, Cell.
[28] S. Priori,et al. Low penetrance in the long-QT syndrome: clinical impact. , 1999, Circulation.
[29] W. Lederer,et al. Defective excitation-contraction coupling in experimental cardiac hypertrophy and heart failure. , 1997, Science.
[30] P. Greengard,et al. Characterization of the interaction between DARPP-32 and protein phosphatase 1 (PP-1): DARPP-32 peptides antagonize the interaction of PP-1 with binding proteins. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[31] 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.
[32] J. Vandenbroucke,et al. QT Interval Prolongation Predicts Cardiovascular Mortality in an Apparently Healthy Population , 1991, Circulation.
[33] P. Schwartz,et al. Idiopathic long QT syndrome: progress and questions. , 1985, American heart journal.
[34] A. Malliani,et al. The long Q-T syndrome. , 1975, American heart journal.