N. Epstein

发表

Mutations in either the essential or regulatory light chains of myosin are associated with a rare myopathy in human heart and skeletal muscle

I. Rayment, K. Poetter, He Jiang, 1996, Nature Genetics.

Adaptive postprocessing techniques for myocardial tissue tracking with displacement-encoded MR imaging.

Kwame S. Kutten, H. Wen, P. Croisille, 2008, Radiology.

Magnetic resonance imaging assessment of myocardial elastic modulus and viscosity using displacement imaging and phase‐contrast velocity mapping

Han Wen, H. Wen, N. Epstein, 2005, Magnetic resonance in medicine.

Left ventricular form and function: scientific priorities and strategic planning for development of new views of disease.

Andrew D McCulloch, Francisco Torrent-Guasp, Mark Doyle, 2004, Circulation.

Prevalence of hypertrophic cardiomyopathy and limitations of screening methods.

L. Fananapazir, N. Epstein, 1995, Circulation.

Relationship of the C242T p22phox gene polymorphism to angiographic coronary artery disease and endothelial function.

A. Quyyumi, N. Epstein, T. Finkel, 1999, American journal of medical genetics.

The insertion/deletion polymorphism of the angiotensin-converting enzyme gene determines coronary vascular tone and nitric oxide activity.

A. Quyyumi, N. Epstein, M. Waclawiw, 2000, Journal of the American College of Cardiology.

Contribution of bradykinin receptor dysfunction to abnormal coronary vasomotion in humans.

A. Quyyumi, N. Epstein, W. Schenke, 2000, Journal of the American College of Cardiology.

Genetic evidence of dissociation (generational skips) of electrical from morphologic forms of hypertrophic cardiomyopathy.

L. Fananapazir, N. Epstein, H. J. Lin, 1990, The American journal of cardiology.

Cellules souches se transformant en cardiomyocytes a battements spontanes

T. V. Gopal, S. Hassanzadeh, N. Epstein, 2002 .

Association Between Polymorphism in the Chemokine Receptor CX3CR1 and Coronary Vascular Endothelial Dysfunction and Atherosclerosis

A. Quyyumi, N. Epstein, D. McDermott, 2001, Circulation research.

Structural and functional responses of mammalian thick filaments to alterations in myosin regulatory light chains.

J. Stull, L. Fananapazir, N. Epstein, 1998, Journal of structural biology.

Evidence of Genetic Heterogeneity in Five Kindreds With Familial Hypertrophic Cardiomyopathy

J. Lalouel, R. Lifton, L. Fananapazir, 1992, Circulation.

Genotype-Phenotpe Correlations in Hypertrophic Cardiomyopathy Insights Provided by Comparisons of Kindreds With Distinct and Identical j3-Myosin Heavy Chain Gene Mutations

L. Fananapazir, N. Epstein, 2005 .

Structural interpretation of the mutations in the beta-cardiac myosin that have been implicated in familial hypertrophic cardiomyopathy.

I. Rayment, J. Sellers, L. Fananapazir, 1995, Proceedings of the National Academy of Sciences of the United States of America.

Sensing Stretch Is Fundamental

N. Epstein, Julien S. Davis, 2003, Cell.

Skeletal muscle expression and abnormal function of beta-myosin in hypertrophic cardiomyopathy.

W. Zhu, J. Sellers, L. Fananapazir, 1993, The Journal of clinical investigation.

Missense mutations in the beta-myosin heavy-chain gene cause central core disease in hypertrophic cardiomyopathy.

M. Dalakas, L. Fananapazir, N. Epstein, 1993, Proceedings of the National Academy of Sciences of the United States of America.

Common miR-590 Variant rs6971711 Present Only in African Americans Reduces miR-590 Biogenesis

Celia P. Corona-Villalobos, T. Abraham, N. Epstein, 2016, PloS one.

Differences in Clinical Expression of Hypertrophic Cardiomyopathy Associated With Two Distinct Mutations in the β‐Myosin Heavy Chain Gene: A 908Leu→Val Mutation and a 403Arg→gGln Mutation

L. Fananapazir, N. Epstein, G. Cohn, 1992, Circulation.

Long‐term Results of Dual‐Chamber (DDD) Pacing in Obstructive Hypertrophic Cardiomyopathy: Evidence for Progressive Symptomatic and Hemodynamic Improvement and Reduction of Left Ventricular Hypertrophy

D Tripodi, L. Fananapazir, N. Epstein, 1994, Circulation.

Insertion-deletion polymorphism of the ACE gene modulates reversibility of endothelial dysfunction with ACE inhibition.

A. Quyyumi, N. Epstein, M. Waclawiw, 2000, Circulation.

Adult Murine Skeletal Muscle Contains Cells That Can Differentiate into Beating Cardiomyocytes In Vitro

T. V. Gopal, M. Rogawski, S. Hassanzadeh, 2005, PLoS biology.

The Overall Pattern of Cardiac Contraction Depends on a Spatial Gradient of Myosin Regulatory Light Chain Phosphorylation

H. Wen, A. Aletras, S. Hassanzadeh, 2001, Cell.

The in vitro motility activity of β-cardiac myosin depends on the nature of the β-myosin heavy chain gene mutation in hypertrophic cardiomyopathy

J. Sellers, L. Fananapazir, N. Epstein, 1997, Journal of Muscle Research & Cell Motility.

Abnormal contractile properties of muscle fibers expressing beta-myosin heavy chain gene mutations in patients with hypertrophic cardiomyopathy.

L. Fananapazir, N. Epstein, H. Sweeney, 1995, The Journal of clinical investigation.

The in vitro motility activity of beta-cardiac myosin depends on the nature of the beta-myosin heavy chain gene mutation in hypertrophic cardiomyopathy.

J. Sellers, L. Fananapazir, N. Epstein, 1997, Journal of muscle research and cell motility.

The stretch-activation response may be critical to the proper functioning of the mammalian heart.

V. Ferrans, K. Poetter, S. Hassanzadeh, 1999, Proceedings of the National Academy of Sciences of the United States of America.

When is a fly in the ointment a solution and not a problem?

N. Epstein, Julien S. Davis, 2006, Circulation research.

A gradient of myosin regulatory light-chain phosphorylation across the ventricular wall supports cardiac torsion.

A. Aletras, S. Hassanzadeh, N. Epstein, 2002, Cold Spring Harbor symposia on quantitative biology.

Investigation and Clinical Significance of Arrhythmias in Patients with Hypertrophic Cardiomyopathy

S. Epstein, L. Fananapazir, N. Epstein, 1991 .

Genotype-phenotype correlations in hypertrophic cardiomyopathy. Insights provided by comparisons of kindreds with distinct and identical beta-myosin heavy chain gene mutations.

L. Fananapazir, N. Epstein, 1994, Circulation.

Development of New Views of Disease Left Ventricular Form and Function : Scientific Priorities and Strategic Planning for

Andrew D. McCulloch, Neil B. Ingels, Francisco Torrent-Guasp, 2013 .

Kinetic effects of myosin regulatory light chain phosphorylation on skeletal muscle contraction.

N. Epstein, Julien S. Davis, Colleen L. Satorius, 2002, Biophysical journal.

The molecular biology and pathophysiology of hypertrophic cardiomyopathy due to mutations in the beta myosin heavy chains and the essential and regulatory light chains.

N. Epstein, 1998, Advances in experimental medicine and biology.

Kinetic effects of fiber type on the two subcomponents of the Huxley-Simmons phase 2 in muscle.

N. Epstein, Julien S. Davis, 2003, Biophysical journal.