Prakash C Viswanathan

Summary

Affiliation: Vanderbilt University
Country: USA

Publications

  1. pmc Mutation in glycerol-3-phosphate dehydrogenase 1 like gene (GPD1-L) decreases cardiac Na+ current and causes inherited arrhythmias
    Barry London
    Cardiovascular Institute, University of Pittsburgh Medical Center, Scaife S 572, 200 Lothrop St, Pittsburgh, PA 15213 2582, USA
    Circulation 116:2260-8. 2007
  2. pmc Sex, age, and regional differences in L-type calcium current are important determinants of arrhythmia phenotype in rabbit hearts with drug-induced long QT type 2
    Carl Sims
    University of Pittsburgh, School of Medicine, Department of Cell Biology and Physiology, Pittsburgh, PA 15261, USA
    Circ Res 102:e86-100. 2008
  3. ncbi request reprint Inherited sodium channelopathies: a continuum of channel dysfunction
    Prakash C Viswanathan
    Department of Anesthesiology, Room 560, Preston Research Building, Vanderbilt University School of Medicine, 2220 Pierce Avenue, Nashville, TN 37232 6602, USA
    Trends Cardiovasc Med 14:28-35. 2004
  4. ncbi request reprint New mechanism contributing to drug-induced arrhythmia: rescue of a misprocessed LQT3 mutant
    Kai Liu
    Departments of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
    Circulation 112:3239-46. 2005
  5. pmc Functional Interactions between Distinct Sodium Channel Cytoplasmic Domains through the Action of Calmodulin
    Franck Potet
    Departments of Anesthesiology, Pharmacology, Medicine, Biochemistry, and Chemistry and Center for Structural Biology, Vanderbilt University, Nashville, Tennessee 37232, USA
    J Biol Chem 284:8846-54. 2009
  6. pmc A common SCN5A polymorphism modulates the biophysical effects of an SCN5A mutation
    Prakash C Viswanathan
    Department of Anesthesiology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    J Clin Invest 111:341-6. 2003
  7. ncbi request reprint Quantitation of protein kinase A-mediated trafficking of cardiac sodium channels in living cells
    Haifa Hallaq
    Department of Medicine, Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232 6602, USA
    Cardiovasc Res 72:250-61. 2006
  8. ncbi request reprint HERG is protected from pharmacological block by alpha-1,2-glucosyltransferase function
    Tadashi Nakajima
    Department of Anesthesiology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232 6602, USA
    J Biol Chem 282:5506-13. 2007
  9. pmc Genetics of acquired long QT syndrome
    Dan M Roden
    Department of Medicine, Oates Institute for Experimental Therapeutics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    J Clin Invest 115:2025-32. 2005
  10. ncbi request reprint Oxidative mediated lipid peroxidation recapitulates proarrhythmic effects on cardiac sodium channels
    Koji Fukuda
    Department of Anesthesiology, Vanderbilt University School of Medicine, Nashville, TN, USA
    Circ Res 97:1262-9. 2005

Collaborators

Detail Information

Publications14

  1. pmc Mutation in glycerol-3-phosphate dehydrogenase 1 like gene (GPD1-L) decreases cardiac Na+ current and causes inherited arrhythmias
    Barry London
    Cardiovascular Institute, University of Pittsburgh Medical Center, Scaife S 572, 200 Lothrop St, Pittsburgh, PA 15213 2582, USA
    Circulation 116:2260-8. 2007
    ..We previously used positional cloning to identify a new locus on chromosome 3p24 in a large family with Brugada syndrome and excluded SCN5A as a candidate gene...
  2. pmc Sex, age, and regional differences in L-type calcium current are important determinants of arrhythmia phenotype in rabbit hearts with drug-induced long QT type 2
    Carl Sims
    University of Pittsburgh, School of Medicine, Department of Cell Biology and Physiology, Pittsburgh, PA 15261, USA
    Circ Res 102:e86-100. 2008
    ....
  3. ncbi request reprint Inherited sodium channelopathies: a continuum of channel dysfunction
    Prakash C Viswanathan
    Department of Anesthesiology, Room 560, Preston Research Building, Vanderbilt University School of Medicine, 2220 Pierce Avenue, Nashville, TN 37232 6602, USA
    Trends Cardiovasc Med 14:28-35. 2004
    ..These new insights enhance understanding of the structure-function relationships of voltage-gated Na+ channels, and also highlight the complexities involved in linking single mutations, ion-channel behavior, and cardiac rhythm...
  4. ncbi request reprint New mechanism contributing to drug-induced arrhythmia: rescue of a misprocessed LQT3 mutant
    Kai Liu
    Departments of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
    Circulation 112:3239-46. 2005
    ..To address this discrepancy, we tested the hypothesis that this mutant channel is not processed normally...
  5. pmc Functional Interactions between Distinct Sodium Channel Cytoplasmic Domains through the Action of Calmodulin
    Franck Potet
    Departments of Anesthesiology, Pharmacology, Medicine, Biochemistry, and Chemistry and Center for Structural Biology, Vanderbilt University, Nashville, Tennessee 37232, USA
    J Biol Chem 284:8846-54. 2009
    ..These findings have bearing upon Na(+) channel function in genetically altered channels and under pathophysiologic conditions where [Ca(2+)](i) impacts cardiac conduction...
  6. pmc A common SCN5A polymorphism modulates the biophysical effects of an SCN5A mutation
    Prakash C Viswanathan
    Department of Anesthesiology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    J Clin Invest 111:341-6. 2003
    ..The mutation and the polymorphism were both found in the same allele of a child with isolated conduction disease, suggesting a direct functional association between a polymorphism and a mutation in the same gene...
  7. ncbi request reprint Quantitation of protein kinase A-mediated trafficking of cardiac sodium channels in living cells
    Haifa Hallaq
    Department of Medicine, Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232 6602, USA
    Cardiovasc Res 72:250-61. 2006
    ....
  8. ncbi request reprint HERG is protected from pharmacological block by alpha-1,2-glucosyltransferase function
    Tadashi Nakajima
    Department of Anesthesiology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232 6602, USA
    J Biol Chem 282:5506-13. 2007
    ..Incorporation of in vitro data into a computational model indicated that KCR1 expression is protective against arrhythmias. These findings reveal a potential new avenue for targeted prevention of aLQTS...
  9. pmc Genetics of acquired long QT syndrome
    Dan M Roden
    Department of Medicine, Oates Institute for Experimental Therapeutics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    J Clin Invest 115:2025-32. 2005
    ....
  10. ncbi request reprint Oxidative mediated lipid peroxidation recapitulates proarrhythmic effects on cardiac sodium channels
    Koji Fukuda
    Department of Anesthesiology, Vanderbilt University School of Medicine, Nashville, TN, USA
    Circ Res 97:1262-9. 2005
    ..These data suggest Na+ channel dysfunction evoked by lipid peroxidation is a candidate mechanism for ischemia-related conduction abnormalities and arrhythmias...
  11. ncbi request reprint Allelic variants in long-QT disease genes in patients with drug-associated torsades de pointes
    Ping Yang
    Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tenn 37232, USA
    Circulation 105:1943-8. 2002
    ..We have previously identified functionally important DNA variants in genes encoding K+ channel ancillary subunits in 11% of an aLQTS cohort...
  12. pmc Compound-specific Na+ channel pore conformational changes induced by local anaesthetics
    Koji Fukuda
    Department of Anaesthesiology, Vanderbilt University, School of Medicine, Nashville, TN 37232 6602, USA
    J Physiol 564:21-31. 2005
    ..Our findings suggest that LA compounds may produce their kinetically distinct voltage-dependent behaviour by modulating slow inactivation gating to varying degrees...
  13. ncbi request reprint Clinical, genetic, and biophysical characterization of SCN5A mutations associated with atrioventricular conduction block
    Dao W Wang
    Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, Tenn, and Department of Pediatrics, Medical University of South Carolina, Charleston, USA
    Circulation 105:341-6. 2002
    ..The mutations also reduce sodium current density and enhance slower inactivation components. Action potential simulations predict that this combination of biophysical abnormalities will significantly slow myocardial conduction velocity...
  14. pmc A sodium channel pore mutation causing Brugada syndrome
    Arnold E Pfahnl
    Division of Cardiology, Atlanta Veterans Affairs Medical Center and Emory University, Atlanta, Georgia 30033, USA
    Heart Rhythm 4:46-53. 2007
    ..Both male and female carriers are symptomatic at young ages, have typical Brugada-type electrocardiogram changes, and have relatively normal corrected QT intervals...