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1
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Winitsky SO, Gopal TV, Hassanzadeh S, Takahashi H, Gryder D, Rogawski MA, Takeda K, Yu ZX, Xu YH, Epstein ND.
Adult murine skeletal muscle contains cells that can differentiate into beating cardiomyocytes in vitro.
PLoS Biol 3(4): e87, 2005.
[Text Abstract on PubMed]
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2
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Buckberg GD, Weisfeldt ML, Ballester M, Beyar R, Burkhoff D, Coghlan HC, Doyle M, Epstein ND, Gharib M, Ideker RE, Ingels NB, LeWinter MM, McCulloch AD, Pohost GM, Reinlib LJ, Sahn DJ, Sopko G, Spinale FG, Spotnitz HM, Torrent-Guasp F, Shapiro EP.
Left ventricular form and function: scientific priorities and strategic planning for development of new views of disease.
Circulation 110(14): e333-6, 2004.
[Text Abstract on PubMed]
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3
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Davis JS, Epstein ND.
Kinetic effects of fiber type on the two subcomponents of the Huxley-Simmons phase 2 in muscle.
Biophys J 85(1): 390-401, 2003.
[Text Abstract on PubMed]
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4
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Epstein ND, Davis JS.
Sensing stretch is fundamental.
Cell 112(2): 147-50, 2003.
[Text Abstract on PubMed]
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5
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Davis JS, Hassanzadeh S, Winitsky S, Wen H, Aletras A, Epstein ND.
A gradient of myosin regulatory light-chain phosphorylation across the ventricular wall supports cardiac torsion.
Cold Spring Harb Symp Quant Biol 67: 345-52, 2002.
[Text Abstract on PubMed]
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6
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Davis JS, Satorius CL, Epstein ND.
Kinetic effects of myosin regulatory light chain phosphorylation on skeletal muscle contraction.
Biophys J 83(1): 359-70, 2002.
[Text Abstract on PubMed]
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7
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Davis JS, Hassanzadeh S, Winitsky S, Lin H, Satorius C, Vemuri R, Aletras AH, Wen H, Epstein ND.
The overall pattern of cardiac contraction depends on a spatial gradient of myosin regulatory light chain phosphorylation.
Cell 107(5): 631-41, 2001.
[Text Abstract on PubMed]
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8
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Vemuri R, Lankford EB, Poetter K, Hassanzadeh S, Takeda K, Yu ZX, Ferrans VJ, Epstein ND.
The stretch-activation response may be critical to the proper functioning of the mammalian heart.
Proc Natl Acad Sci U S A 96(3): 1048-53, 1999.
[Text Abstract on PubMed]
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9
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Epstein ND.
The molecular biology and pathophysiology of hypertrophic cardiomyopathy due to mutations in the beta myosin heavy chains and the essential and regulatory light chains.
Adv Exp Med Biol 453: 105-14; discussion 114-5, 1998.
[Text Abstract on PubMed]
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10
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Levine RJ, Yang Z, Epstein ND, Fananapazir L, Stull JT, Sweeney HL.
Structural and functional responses of mammalian thick filaments to alterations in myosin regulatory light chains.
J Struct Biol 122(1-2): 149-61, 1998.
[Text Abstract on PubMed]
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11
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Cuda G, Fananapazir L, Epstein ND, Sellers JR.
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 Muscle Res Cell Motil 18(3): 275-83, 1997.
[Text Abstract on PubMed]
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12
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Yang CC, Xiao X, Zhu X, Ansardi DC, Epstein ND, Frey MR, Matera AG, Samulski RJ.
Cellular recombination pathways and viral terminal repeat hairpin structures are sufficient for adeno-associated virus integration in vivo and in vitro.
J Virol 71(12): 9231-47, 1997.
[Text Abstract on PubMed]
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13
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Poetter K, Jiang H, Hassanzadeh S, Master SR, Chang A, Dalakas MC, Rayment I, Sellers JR, Fananapazir L, Epstein ND.
Mutations in either the essential or regulatory light chains of myosin are associated with a rare myopathy in human heart and skeletal muscle.
Nat Genet 13(1): 63-9, 1996.
[Text Abstract on PubMed]
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14
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Lankford EB, Epstein ND, Fananapazir L, Sweeney HL.
Abnormal contractile properties of muscle fibers expressing beta-myosin heavy chain gene mutations in patients with hypertrophic cardiomyopathy.
J Clin Invest 95(3): 1409-14, 1995.
[Text Abstract on PubMed]
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15
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Rayment I, Holden HM, Sellers JR, Fananapazir L, Epstein ND.
Structural interpretation of the mutations in the beta-cardiac myosin that have been implicated in familial hypertrophic cardiomyopathy.
Proc Natl Acad Sci U S A 92(9): 3864-8, 1995.
[Text Abstract on PubMed]
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16
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Fananapazir L, Epstein ND, Curiel RV, Panza JA, Tripodi D, McAreavey D.
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.
Circulation 90(6): 2731-42, 1994.
[Text Abstract on PubMed]
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17
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Fananapazir L, Epstein ND.
Genotype-phenotype correlations in hypertrophic cardiomyopathy. Insights provided by comparisons of kindreds with distinct and identical beta-myosin heavy chain gene mutations.
Circulation 89(1): 22-32, 1994.
[Text Abstract on PubMed]
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18
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Cuda G, Fananapazir L, Zhu WS, Sellers JR, Epstein ND.
Skeletal muscle expression and abnormal function of beta-myosin in hypertrophic cardiomyopathy.
J Clin Invest 91(6): 2861-5, 1993.
[Text Abstract on PubMed]
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19
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Fananapazir L, Dalakas MC, Cyran F, Cohn G, Epstein ND.
Missense mutations in the beta-myosin heavy-chain gene cause central core disease in hypertrophic cardiomyopathy.
Proc Natl Acad Sci U S A 90(9): 3993-7, 1993.
[Text Abstract on PubMed]
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20
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Kenney RT, Malech HL, Epstein ND, Roberts RL, Leto TL.
Characterization of the p67phox gene: genomic organization and restriction fragment length polymorphism analysis for prenatal diagnosis in chronic granulomatous disease.
Blood 82(12): 3739-44, 1993.
[Text Abstract on PubMed]
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21
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Epstein ND, Cohn GM, Cyran F, Fananapazir L.
Differences in clinical expression of hypertrophic cardiomyopathy associated with two distinct mutations in the beta-myosin heavy chain gene. A 908Leu----Val mutation and a 403Arg----Gln mutation.
Circulation 86(2): 345-52, 1992.
[Text Abstract on PubMed]
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22
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Epstein ND, Fananapazir L, Lin HJ, Mulvihill J, White R, Lalouel JM, Lifton RP, Nienhuis AW, Leppert M.
Evidence of genetic heterogeneity in five kindreds with familial hypertrophic cardiomyopathy.
Circulation 85(2): 635-47, 1992.
[Text Abstract on PubMed]
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23
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Brook JD, Knight SJ, Roberts SH, Harley HG, Walsh KV, Rundle SA, Freyne K, Koch MC, Epstein ND, Wieringa B.
The physical map of chromosome arm 19q: some new assignments, confirmations and re-assessments.
Hum Genet 87(1): 65-72, 1991.
[Text Abstract on PubMed]
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24
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Epstein ND, Lin HJ, Fananapazir L.
Genetic evidence of dissociation (generational skips) of electrical from morphologic forms of hypertrophic cardiomyopathy.
Am J Cardiol 66(5): 627-31, 1990.
[Text Abstract on PubMed]
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