Robert Kass

Summary

Affiliation: Columbia University
Country: USA

Publications

  1. pmc Common molecular determinants of flecainide and lidocaine block of heart Na+ channels: evidence from experiments with neutral and quaternary flecainide analogues
    Huajun Liu
    Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA
    J Gen Physiol 121:199-214. 2003
  2. pmc The Na+ channel inactivation gate is a molecular complex: a novel role of the COOH-terminal domain
    Howard K Motoike
    Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA
    J Gen Physiol 123:155-65. 2004
  3. pmc A novel and lethal de novo LQT-3 mutation in a newborn with distinct molecular pharmacology and therapeutic response
    John R Bankston
    Department of Pharmacology, College of Physicians and Surgeons, Columbia University Medical Center, New York, New York, United States of America
    PLoS ONE 2:e1258. 2007
  4. pmc Channel openings are necessary but not sufficient for use-dependent block of cardiac Na(+) channels by flecainide: evidence from the analysis of disease-linked mutations
    Huajun Liu
    Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA
    J Gen Physiol 120:39-51. 2002
  5. pmc Characterization of KCNQ1 atrial fibrillation mutations reveals distinct dependence on KCNE1
    Priscilla J Chan
    Department of Pharmacology, Columbia University Medical Center, New York, NY 10032, USA
    J Gen Physiol 139:135-44. 2012
  6. pmc Induced pluripotent stem cells used to reveal drug actions in a long QT syndrome family with complex genetics
    Cecile Terrenoire
    Department of Pharmacology, College of Physicians and Surgeons, Columbia University Medical Center, New York, NY 10032, USA
    J Gen Physiol 141:61-72. 2013
  7. pmc Perturbation of sodium channel structure by an inherited Long QT Syndrome mutation
    Ian W Glaaser
    Department of Pharmacology, College of Physicians and Surgeons of Columbia University, Columbia University Medical Center, 630 W 168th Street, New York, NY 10032, USA
    Nat Commun 3:706. 2012
  8. pmc TEA(+)-sensitive KCNQ1 constructs reveal pore-independent access to KCNE1 in assembled I(Ks) channels
    J Kurokawa
    Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA
    J Gen Physiol 117:43-52. 2001
  9. ncbi request reprint Sodium channel inactivation in heart: a novel role of the carboxy-terminal domain
    Robert S Kass
    Department of Pharmacology, Columbia University, New York, New York 10032, USA
    J Cardiovasc Electrophysiol 17:S21-S25. 2006
  10. ncbi request reprint Pharmacogenomics in the treatment of epilepsy
    Colleen E Clancy
    Department of Pharmacology, Columbia University, College of Physicians and Surgeons, 630 W 168th Street, New York, NY 10032, USA
    Pharmacogenomics 4:747-51. 2003

Collaborators

Detail Information

Publications62

  1. pmc Common molecular determinants of flecainide and lidocaine block of heart Na+ channels: evidence from experiments with neutral and quaternary flecainide analogues
    Huajun Liu
    Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA
    J Gen Physiol 121:199-214. 2003
    ..The data also suggest that the two drugs share a common receptor but, consistent with the modulated receptor hypothesis, reach this receptor by distinct routes dictated by the degree of ionization of the drug molecules...
  2. pmc The Na+ channel inactivation gate is a molecular complex: a novel role of the COOH-terminal domain
    Howard K Motoike
    Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA
    J Gen Physiol 123:155-65. 2004
    ....
  3. pmc A novel and lethal de novo LQT-3 mutation in a newborn with distinct molecular pharmacology and therapeutic response
    John R Bankston
    Department of Pharmacology, College of Physicians and Surgeons, Columbia University Medical Center, New York, New York, United States of America
    PLoS ONE 2:e1258. 2007
    ....
  4. pmc Channel openings are necessary but not sufficient for use-dependent block of cardiac Na(+) channels by flecainide: evidence from the analysis of disease-linked mutations
    Huajun Liu
    Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA
    J Gen Physiol 120:39-51. 2002
    ..Analysis of flecainide block of mutant channels linked to these rare disorders has provided novel insight into the molecular determinants of drug action...
  5. pmc Characterization of KCNQ1 atrial fibrillation mutations reveals distinct dependence on KCNE1
    Priscilla J Chan
    Department of Pharmacology, Columbia University Medical Center, New York, NY 10032, USA
    J Gen Physiol 139:135-44. 2012
    ....
  6. pmc Induced pluripotent stem cells used to reveal drug actions in a long QT syndrome family with complex genetics
    Cecile Terrenoire
    Department of Pharmacology, College of Physicians and Surgeons, Columbia University Medical Center, New York, NY 10032, USA
    J Gen Physiol 141:61-72. 2013
    ....
  7. pmc Perturbation of sodium channel structure by an inherited Long QT Syndrome mutation
    Ian W Glaaser
    Department of Pharmacology, College of Physicians and Surgeons of Columbia University, Columbia University Medical Center, 630 W 168th Street, New York, NY 10032, USA
    Nat Commun 3:706. 2012
    ..These data provide a structural correlation to the pathological phenotype of the mutant channel...
  8. pmc TEA(+)-sensitive KCNQ1 constructs reveal pore-independent access to KCNE1 in assembled I(Ks) channels
    J Kurokawa
    Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA
    J Gen Physiol 117:43-52. 2001
    ....
  9. ncbi request reprint Sodium channel inactivation in heart: a novel role of the carboxy-terminal domain
    Robert S Kass
    Department of Pharmacology, Columbia University, New York, New York 10032, USA
    J Cardiovasc Electrophysiol 17:S21-S25. 2006
    ..Disruption of this interaction leads to persistent sodium channel current, action potential prolongation, and elevated risk of cardiac arrhythmia...
  10. ncbi request reprint Pharmacogenomics in the treatment of epilepsy
    Colleen E Clancy
    Department of Pharmacology, Columbia University, College of Physicians and Surgeons, 630 W 168th Street, New York, NY 10032, USA
    Pharmacogenomics 4:747-51. 2003
    ..The investigation of relationships between genotype and patient responses to drug treatment is termed pharmacogenomics...
  11. pmc Long QT syndrome: novel insights into the mechanisms of cardiac arrhythmias
    Robert S Kass
    Department of Pharmacology, Columbia University College of Physicians and Surgeons, 630 West 168th Street, P and S 7 401, New York, New York 10032, USA
    J Clin Invest 112:810-5. 2003
    ..Discovery and analysis of gene mutations associated with variants of this disorder have provided novel insight into mechanisms of cardiac arrhythmia and have raised the possibility of mutation-specific therapeutic intervention...
  12. ncbi request reprint Leucine/isoleucine zipper coordination of ion channel macromolecular signaling complexes in the heart. Roles in inherited arrhythmias
    R S Kass
    Department of Pharmacology Division of Cardiology, College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY 10032, USA
    Trends Cardiovasc Med 13:52-6. 2003
    ..Disruption of local signaling by disease-associated LIZ mutations unbalances the physiologic response to SNS stimulation and increases the risk of arrhythmia in mutation carriers...
  13. pmc The channelopathies: novel insights into molecular and genetic mechanisms of human disease
    Robert S Kass
    Department of Pharmacology, Columbia University Medical Center, New York, New York 10032, USA
    J Clin Invest 115:1986-9. 2005
    ..This series of reviews examines the roles of ion channels in health and disease...
  14. pmc Biophysical properties of slow potassium channels in human embryonic stem cell derived cardiomyocytes implicate subunit stoichiometry
    Kai Wang
    Department of Pharmacology, College of Physicians and Surgeons, Columbia University Medical Center, New York, NY 10032, USA
    J Physiol 589:6093-104. 2011
    ..This establishes a new baseline for I(Ks) channel properties in myocytes derived from pluripotent stem cells and will guide future studies in patient-specific hiPSCs...
  15. ncbi request reprint A novel LQT-3 mutation disrupts an inactivation gate complex with distinct rate-dependent phenotypic consequences
    John R Bankston
    Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA
    Channels (Austin) 1:273-80. 2007
    ....
  16. ncbi request reprint Non-equilibrium gating in cardiac Na+ channels: an original mechanism of arrhythmia
    Colleen E Clancy
    Department of Pharmacology, Columbia University College of Physicians and Surgeons, 630 W 168th St, New York, NY 10032, USA
    Circulation 107:2233-7. 2003
    ..1% of peak) compared with wild-type (WT) channels. In fact, it is difficult to reconcile the seemingly innocuous kinetic alterations in I1768V as measured during standard protocols under steady-state conditions with the disease phenotype...
  17. pmc Defective cardiac ion channels: from mutations to clinical syndromes
    Colleen E Clancy
    Department of Pharmacology, Columbia University, 630 West 168th Street, New York, New York 10032, USA
    J Clin Invest 110:1075-7. 2002
  18. ncbi request reprint Autonomic control of cardiac action potentials: role of potassium channel kinetics in response to sympathetic stimulation
    Cecile Terrenoire
    Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA
    Circ Res 96:e25-34. 2005
    ..The full text of this article is available online at http://circres.ahajournals.org...
  19. ncbi request reprint Role of sodium channels in propagation in heart muscle: how subtle genetic alterations result in major arrhythmic disorders
    Cecile Terrenoire
    Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA
    J Cardiovasc Electrophysiol 18:900-5. 2007
    ..The improved understanding of the mechanisms leading to these cardiac arrhythmic events represents a first step in the development of therapeutic treatments...
  20. pmc Molecular basis of ranolazine block of LQT-3 mutant sodium channels: evidence for site of action
    Sandra Fredj
    Department of Pharmacology, Columbia University Medical Center, New York, NY 10032, USA
    Br J Pharmacol 148:16-24. 2006
    ....
  21. ncbi request reprint K+ channel structure-activity relationships and mechanisms of drug-induced QT prolongation
    Colleen E Clancy
    Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
    Annu Rev Pharmacol Toxicol 43:441-61. 2003
    ..Drug-induced disruption of cellular repolarization underlies electrocardiographic abnormalities that are diagnostic indicators of arrhythmia susceptibility...
  22. pmc Theoretical investigation of the neuronal Na+ channel SCN1A: abnormal gating and epilepsy
    Colleen E Clancy
    Department of Pharmacology, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA
    Biophys J 86:2606-14. 2004
    ..This work represents a first step in developing a comprehensive theoretical model to investigate the molecular mechanisms underlying runaway excitation that cause epilepsy...
  23. ncbi request reprint Mutations in cardiac sodium channels: clinical implications
    Huajun Liu
    Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
    Am J Pharmacogenomics 3:173-9. 2003
    ....
  24. ncbi request reprint A carboxyl-terminal hydrophobic interface is critical to sodium channel function. Relevance to inherited disorders
    Ian W Glaaser
    Department of Pharmacology, Columbia University, New York, New York 10032, USA
    J Biol Chem 281:24015-23. 2006
    ..We thus demonstrate a novel role of the sodium channel COOH terminus structure in the control of channel inactivation and in pathologies caused by inherited mutations that disrupt it...
  25. ncbi request reprint Inherited and acquired vulnerability to ventricular arrhythmias: cardiac Na+ and K+ channels
    Colleen E Clancy
    Department of Physiology and Biophysics, Institute for Computational Biomedicine, Weill Medical College of Cornell University, New York, New York 10021, USA
    Physiol Rev 85:33-47. 2005
    ..Improving understanding of abnormalities may provide a basis for the development of therapeutic approaches...
  26. ncbi request reprint Modulation of cardiac sodium channel gating by protein kinase A can be altered by disease-linked mutation
    Michihiro Tateyama
    Department of Pharmacology, College of Physicians and Surgeons of Columbia University, 630 W 168th Street, New York, NY 10032, USA
    J Biol Chem 278:46718-26. 2003
    ....
  27. pmc Insights into the molecular mechanisms of bradycardia-triggered arrhythmias in long QT-3 syndrome
    Colleen E Clancy
    Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
    J Clin Invest 110:1251-62. 2002
    ..These results link mutation-induced changes in Na+ channel gating mode transitions to heart rate-dependent changes in cellular electrical activity underlying a key LQT-3 clinical phenotype...
  28. ncbi request reprint Requirement of a macromolecular signaling complex for beta adrenergic receptor modulation of the KCNQ1-KCNE1 potassium channel
    Steven O Marx
    Department of Pharmacology, Center for Molecular Cardiology, Department of Medicine, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA
    Science 295:496-9. 2002
    ..Yotiao binds to hKCNQ1 by a leucine zipper motif, which is disrupted by an LQTS mutation (hKCNQ1-G589D). Identification of the hKCNQ1 macromolecular complex provides a mechanism for SNS modulation of cardiac APD through IKS...
  29. pmc Stabilization of cardiac ryanodine receptor prevents intracellular calcium leak and arrhythmias
    Stephan E Lehnart
    Department of Physiology, Clyde and Helen Wu Center for Molecular Cardiology, Columbia University, New York, NY 10032, USA
    Proc Natl Acad Sci U S A 103:7906-10. 2006
    ..Our data suggest that calstabin-2 deficiency is as a critical mediator of triggers that initiate cardiac arrhythmias...
  30. ncbi request reprint Altered Na+ channels promote pause-induced spontaneous diastolic activity in long QT syndrome type 3 myocytes
    Sandra Fredj
    Department of Pharmacology, Columbia University Medical Center, New York, NY 10032, USA
    Circ Res 99:1225-32. 2006
    ....
  31. ncbi request reprint A novel SCN5A mutation associated with long QT-3: altered inactivation kinetics and channel dysfunction
    Ilaria Rivolta
    Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA
    Physiol Genomics 10:191-7. 2002
    ..The effect of these alterations in channel gating results in an increase in window current that may act to disrupt cardiac repolarization...
  32. pmc Mutation of an A-kinase-anchoring protein causes long-QT syndrome
    Lei Chen
    Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA
    Proc Natl Acad Sci U S A 104:20990-5. 2007
    ..Thus, we have demonstrated a link between genetic perturbations in AKAP and human disease in general and AKAP9 and LQTS in particular...
  33. ncbi request reprint Mechanisms of genetic arrhythmias: from DNA to ECG
    Ian W Glaaser
    Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
    Prog Cardiovasc Dis 46:259-70. 2003
    ..Additionally, phenotypically opposite and overlapping cardiac arrhythmogenic syndromes can even stem from the same mutation. Accordingly, the relationship between genetic mutations and clinical syndromes is becoming increasingly complex...
  34. pmc Leaky Ca2+ release channel/ryanodine receptor 2 causes seizures and sudden cardiac death in mice
    Stephan E Lehnart
    Department of Physiology and Cellular Biophysics, Clyde and Helen Wu Center for Molecular Cardiology, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA
    J Clin Invest 118:2230-45. 2008
    ..Based on these data, we propose that CPVT is a combined neurocardiac disorder in which leaky RyR2 channels in the brain cause epilepsy, and the same leaky channels in the heart cause exercise-induced sudden cardiac death...
  35. pmc Molecular determinants of local anesthetic action of beta-blocking drugs: Implications for therapeutic management of long QT syndrome variant 3
    John R Bankston
    Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
    J Mol Cell Cardiol 48:246-53. 2010
    ..Furthermore our results indicate that this activity, like that of local anesthetic drugs, differs both with drug structure and the biophysical changes in Na(+) channel function caused by specific LQT-3 mutations...
  36. pmc Location, location, regulation: a novel role for β-spectrin in the heart
    Kevin J Sampson
    Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, New York, USA
    J Clin Invest 120:3434-7. 2010
    ....
  37. pmc Sodium channel inactivation goes with the flow
    Robert S Kass
    Department of Pharmacology, Columbia University, New York, NY 10027, USA
    J Gen Physiol 124:7-8. 2004
  38. pmc Regulatory actions of the A-kinase anchoring protein Yotiao on a heart potassium channel downstream of PKA phosphorylation
    Junko Kurokawa
    Department of Pharmacology, College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY 10032, USA
    Proc Natl Acad Sci U S A 101:16374-8. 2004
    ..These data reveal previously undescribed actions of Yotiao that occur subsequent to channel phosphorylation and provide evidence that this adaptor protein also may serve as an effector in regulating this important ion channel...
  39. pmc Adrenergic regulation of a key cardiac potassium channel can contribute to atrial fibrillation: evidence from an I Ks transgenic mouse
    Kevin J Sampson
    Department of Pharmacology, Columbia University Medical Center, 630 W 168th St, New York, NY 10032, USA
    J Physiol 586:627-37. 2008
    ....
  40. ncbi request reprint Phosphorylation of the A-kinase-anchoring protein Yotiao contributes to protein kinase A regulation of a heart potassium channel
    Lei Chen
    Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA
    J Biol Chem 280:31347-52. 2005
    ..These results suggest, for the first time, a critical role for the PKA phosphorylation of an AKAP in the functional regulation of an ion channel protein and postphosphorylation allosteric modulation of the I(Ks) channel by Yotiao...
  41. ncbi request reprint Electrophysiological consequences of human IKs channel expression in adult murine heart
    Christine Chiello Tracy
    Department of Pharmacology, Columbia University, College of Physicians and Surgeons, New York, New York 10032, USA
    Am J Physiol Heart Circ Physiol 284:H168-75. 2003
    ..I(Ks) channels impart beta-adrenergic sensitivity to the ventricles and may be responsible for ventricular tachyarrhythmias...
  42. pmc Requirement of subunit expression for cAMP-mediated regulation of a heart potassium channel
    Junko Kurokawa
    Department of Pharmacology, College of Physicians and Surgeons of Columbia University, 630 West 168th Street, New York, NY 10032, USA
    Proc Natl Acad Sci U S A 100:2122-7. 2003
    ..Transduction of protein phosphorylation into physiologically necessary channel function represents a previously uncharacterized role for the KCNE1 auxiliary subunit, which can be disrupted in LQT-5...
  43. pmc The cardiac IKs potassium channel macromolecular complex includes the phosphodiesterase PDE4D3
    Cecile Terrenoire
    Department of Pharmacology, Columbia University Medical Center, New York, New York 10032, USA
    J Biol Chem 284:9140-6. 2009
    ..We conclude that PDE4D3, like protein kinase A and protein phosphatase 1, is recruited to the I(Ks) channel via AKAP-9 and contributes to its critical regulation by cAMP...
  44. pmc Molecular mechanisms of adrenergic stimulation in the heart
    Kevin J Sampson
    Department of Pharmacology, Columbia University, New York, New York 10032, USA
    Heart Rhythm 7:1151-3. 2010
    ..This article briefly reviews the major components of the beta-adrenergic pathway in the heart and discusses the direction of current and future research...
  45. ncbi request reprint Secondary structure of the human cardiac Na+ channel C terminus: evidence for a role of helical structures in modulation of channel inactivation
    Joseph W Cormier
    Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA
    J Biol Chem 277:9233-41. 2002
    ..025% S1885stop (n = 7) versus 0.0028% wild type (n = 9), p < 0.005). These results suggest that the charged structured region of the SCN5A C terminus plays a major role in channel inactivation, stabilizing the inactivated state...
  46. ncbi request reprint Overexpression of beta2-adrenergic receptors cAMP-dependent protein kinase phosphorylates and modulates slow delayed rectifier potassium channels expressed in murine heart: evidence for receptor/channel co-localization
    Keith W Dilly
    Department of Pharmacology, Center for Molecular Cardiology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
    J Biol Chem 279:40778-87. 2004
    ..These data indicate intimate association of KCNQ1 and beta2-ARs and that beta2-AR signaling can modulate the function of IKs channels under conditions of increased beta2-AR expression, even in the absence of exogenous beta-AR agonist...
  47. ncbi request reprint Calmodulin mediates Ca2+ sensitivity of sodium channels
    James Kim
    Department of Pharmacology, Division of Cardiology, Columbia University, New York, New York 10032, USA
    J Biol Chem 279:45004-12. 2004
    ..Together, these data offer new biochemical evidence for Ca2+/CaM modulation of Na+ channel function...
  48. ncbi request reprint Dual roles of the A kinase-anchoring protein Yotiao in the modulation of a cardiac potassium channel: a passive adaptor versus an active regulator
    Lei Chen
    Department of Pharmacology, College of Physicians and Surgeons of Columbia University, 630 W 168th St, New York, NY 10032, USA
    Eur J Cell Biol 85:623-6. 2006
    ..It acts not only as an adaptor protein to coordinate enzymatic reactions but also as an active regulator that directly affects channel function...
  49. pmc Long QT syndrome: from channels to cardiac arrhythmias
    Arthur J Moss
    Heart Research Follow Up Program, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA
    J Clin Invest 115:2018-24. 2005
    ....
  50. ncbi request reprint Molecular physiology of cardiac repolarization
    Jeanne M Nerbonne
    Dept of Molecular Biology and Pharmacology, Washington University Medical School, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Physiol Rev 85:1205-53. 2005
    ....
  51. ncbi request reprint Variable expression of long QT syndrome among gene carriers from families with five different HERG mutations
    Jesaia Benhorin
    Department of Cardiology, Bikur Cholim Hospital, Jerusalem, Israel
    Ann Noninvasive Electrocardiol 7:40-6. 2002
    ..This study assessed the phenotypic variability of LQTS in carriers with the same and with different mutations in the LQT2 gene...
  52. ncbi request reprint Variant of SCN5A sodium channel implicated in risk of cardiac arrhythmia
    Igor Splawski
    Department of Cardiology, Children s Hospital, Harvard Medical School and Howard Hughes Medical Institute, Boston, MA 02115, USA
    Science 297:1333-6. 2002
    ..However, Y1102 may be a useful molecular marker for the prediction of arrhythmia susceptibility in the context of additional acquired risk factors such as the use of certain medications...
  53. ncbi request reprint Proposed diagnostic criteria for the Brugada syndrome: consensus report
    Arthur A M Wilde
    Experimental and Molecular Cardiology Group, Academic Medical Center, Amsterdam, and the Interuniversity Cardiology Institute, The Netherlands
    Circulation 106:2514-9. 2002
  54. ncbi request reprint Clinical, genetic, and electrophysiologic characteristics of a new PAS-domain HERG mutation (M124R) causing Long QT syndrome
    Liat Shushi
    Department of Genetics, The Life Sciences Institute, The Hebrew University, Jerusalem, Israel
    Ann Noninvasive Electrocardiol 10:334-41. 2005
    ..To describe the clinical, genetic, and electrophysiologic characteristics of a new PAS-domain HERG mutation (M124R) that has been identified in a single large Jewish family with Long QT syndrome (LQTS)...
  55. ncbi request reprint Regulation of the voltage-gated cardiac sodium channel Nav1.5 by interacting proteins
    Hugues Abriel
    Department of Pharmacology and Toxicology, Service of Cardiology, University of Lausanne, Bugnon, 27, 1005 Lausanne, Switzerland
    Trends Cardiovasc Med 15:35-40. 2005
    ..5: ankyrin proteins, fibroblast growth factor homologous factor 1B, calmodulin, Nedd4-like ubiquitin-protein ligases, and syntrophin proteins...
  56. ncbi request reprint A novel mutation L619F in the cardiac Na+ channel SCN5A associated with long-QT syndrome (LQT3): a role for the I-II linker in inactivation gating
    Xander H T Wehrens
    Department of Cardiology, Cardiovascular Research Institute Maastricht, The Netherlands
    Hum Mutat 21:552. 2003
    ..Moreover, the defective inactivation imposed by the L619F mutation implies a role for the I-II linker in the Na(+) channel inactivation process...
  57. pmc Mutation of sodium channel SCN3A in a patient with cryptogenic pediatric partial epilepsy
    Katherine D Holland
    Division of Neurology, Cincinnati Children s Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229, USA
    Neurosci Lett 433:65-70. 2008
    ..This observation of a potentially pathogenic mutation of SCN3A (Nav1.3) indicates that this gene should be further evaluated for its contribution to childhood epilepsy...
  58. ncbi request reprint Cardiac voltage-gated sodium channel Nav1.5 is regulated by Nedd4-2 mediated ubiquitination
    Miguel X van Bemmelen
    Department of Pharmacology and Toxicology, University of Lausanne, Switzerland
    Circ Res 95:284-91. 2004
    ..5. These results demonstrate that Na(v)1.5 can be ubiquitinated in heart tissues and that the ubiquitin-protein ligase Nedd4-2 acts on Na(v)1.5 by decreasing the channel density at the cell surface...
  59. ncbi request reprint Novel pore mutation in SCN5A manifests as a spectrum of phenotypes ranging from atrial flutter, conduction disease, and Brugada syndrome to sudden cardiac death
    Tom Rossenbacker
    Center for Transgene Technology and Gene Therapy, Flanders Interuniversitary Institute for Biotechnology, KULeuven, Belgium
    Heart Rhythm 1:610-5. 2004
    ..The purpose of this study was to determine the clinical and biophysical characteristics of a novel SCN5A mutation...
  60. ncbi request reprint A-kinase anchoring proteins: different partners, different dance
    Lei Chen
    Nat Cell Biol 7:1050-1. 2005
  61. ncbi request reprint Fading sodium channels in failing hearts
    John R Bankston
    Circ Res 101:1073-4. 2007
  62. ncbi request reprint Regulation of endocytic recycling of KCNQ1/KCNE1 potassium channels
    Guiscard Seebohm
    Department of Physiology I, University of Tuebingen, Gmelinstrasse 5, D 72076 Tuebingen, Germany
    Circ Res 100:686-92. 2007
    ....

Research Grants37

  1. Molecular Determinants of K+ Channel Regulation in Heart
    Robert Kass; Fiscal Year: 2002
    ..abstract_text> ..
  2. MOLECULAR PHARMACOLOGY OF AN INHERITED HEART DISEASE
    Robert Kass; Fiscal Year: 2005
    ..abstract_text> ..
  3. Molecular Determinants of K+ Channel Regulation in Heart
    Robert Kass; Fiscal Year: 2007
    ..The results of these investigations will provide novel insight into and understanding of the molecular interactions that underlie this fundamental and essential cardiac response. ..
  4. CHARGED DIHYDROPYRIDINES--PROBES OF HEART CA++ CHANNELS
    Robert Kass; Fiscal Year: 2000
    ....
  5. K+ CHANNELS IN NORMAL AND GENETICALLY ALTERED HEART
    Robert Kass; Fiscal Year: 2000
    ..The results of these studies should provide the most detailed description to date of the molecular and genetic properties of IKs and its relevance to human cardiovascular pharmacology and disease. ..
  6. MOLECULAR PHARMACOLOGY OF AN INHERITED HEART DISEASE
    Robert Kass; Fiscal Year: 2000
    ..non-carriers of the LQT-1 and LQT-3 gene mutations to optimize experimental design and therapeutic approaches. ..
  7. K+ CHANNELS IN NORMAL AND GENETICALLY ALTERED HEART
    Robert Kass; Fiscal Year: 1999
    ..The results of these studies should provide the most detailed description to date of the molecular and genetic properties of IKs and its relevance to human cardiovascular pharmacology and disease. ..
  8. MOLECULAR PHARMACOLOGY OF AN INHERITED HEART DISEASE
    Robert Kass; Fiscal Year: 2004
    ..abstract_text> ..
  9. MOLECULAR PHARMACOLOGY OF AN INHERITED HEART DISEASE
    Robert S Kass; Fiscal Year: 2010
    ....
  10. MOLECULAR PHARMACOLOGY OF AN INHERITED HEART DISEASE
    Robert Kass; Fiscal Year: 2009
    ....
  11. MOLECULAR PHARMACOLOGY OF AN INHERITED HEART DISEASE
    Robert Kass; Fiscal Year: 2002
    ..abstract_text> ..
  12. Molecular Determinants of K+ Channel Regulation in Heart
    Robert Kass; Fiscal Year: 2004
    ..abstract_text> ..
  13. TRAINING PROGRAM IN PHARMACOLOGICAL SCIENCES
    Robert Kass; Fiscal Year: 2006
    ..abstract_text> ..
  14. Molecular Determinants of K+ Channel Regulation in Heart
    Robert Kass; Fiscal Year: 2005
    ..The results of these investigations will provide novel insight into and understanding of the molecular interactions that underlie this fundamental and essential cardiac response. ..
  15. MOLECULAR PHARMACOLOGY OF AN INHERITED HEART DISEASE
    Robert Kass; Fiscal Year: 2006
    ..abstract_text> ..
  16. Molecular Determinants of K+ Channel Regulation in Heart
    Robert Kass; Fiscal Year: 2009
    ..The results of these investigations will provide novel insight into and understanding of the molecular interactions that underlie this fundamental and essential cardiac response. ..
  17. MOLECULAR PHARMACOLOGY OF AN INHERITED HEART DISEASE
    Robert Kass; Fiscal Year: 2003
    ..abstract_text> ..
  18. Molecular Determinants of K+ Channel Regulation in Heart
    Robert S Kass; Fiscal Year: 2010
    ..Thus the goal of this work is to define new molecular motifs that are responsible for, and can be targeted to treat, specific congenital cardiac arrhythmias. ..
  19. Molecular Determinants of K+ Channel Regulation in Heart
    Robert Kass; Fiscal Year: 2001
    ..abstract_text> ..
  20. MOLECULAR PHARMACOLOGY OF AN INHERITED HEART DISEASE
    Robert Kass; Fiscal Year: 2001
    ..non-carriers of the LQT-1 and LQT-3 gene mutations to optimize experimental design and therapeutic approaches. ..
  21. Molecular Determinants of K+ Channel Regulation in Heart
    Robert Kass; Fiscal Year: 2003
    ..abstract_text> ..
  22. CHARGED DIHYDROPYRIDINES--PROBES OF HEART CA++ CHANNELS
    Robert Kass; Fiscal Year: 2001
    ....
  23. Molecular Determinants of K+ Channel Regulation in Heart
    Robert Kass; Fiscal Year: 2006
    ..The results of these investigations will provide novel insight into and understanding of the molecular interactions that underlie this fundamental and essential cardiac response. ..
  24. MOLECULAR PHARMACOLOGY OF AN INHERITED HEART DISEASE
    Robert Kass; Fiscal Year: 1999
    ..non-carriers of the LQT-1 and LQT-3 gene mutations to optimize experimental design and therapeutic approaches. ..
  25. CHARGED DIHYDROPYRIDINES--PROBES OF HEART CA++ CHANNELS
    Robert Kass; Fiscal Year: 1999
    ....
  26. MOLECULAR PHARMACOLOGY OF AN INHERITED HEART DISEASE
    Robert Kass; Fiscal Year: 2007
    ....