Inotropic stimulation induces cardiac dysfunction in transgenic mice expressing a troponin T (I79N) mutation linked to familial hypertrophic cardiomyopathy.
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Disease-causing mutations in cardiac troponin T: identification of a critical tropomyosin-binding regionPhosphorylation or glutamic acid substitution at protein kinase C sites on cardiac troponin I differentially depress myofilament tension and shortening velocityTroponin T isoforms and posttranscriptional modifications: Evolution, regulation and functionCasq2 deletion causes sarcoplasmic reticulum volume increase, premature Ca2+ release, and catecholaminergic polymorphic ventricular tachycardiaDecreased energetics in murine hearts bearing the R92Q mutation in cardiac troponin TMyofilament Ca2+ sensitization causes susceptibility to cardiac arrhythmia in mice.Epigallocatechin-3-Gallate Accelerates Relaxation and Ca2+ Transient Decay and Desensitizes Myofilaments in Healthy and Mybpc3-Targeted Knock-in Cardiomyopathic Mice.Investigating the role of uncoupling of troponin I phosphorylation from changes in myofibrillar Ca(2+)-sensitivity in the pathogenesis of cardiomyopathy.Cardiac-specific over-expression of epidermal growth factor receptor 2 (ErbB2) induces pro-survival pathways and hypertrophic cardiomyopathy in mice.Cardiac myosin heavy chain isoform exchange alters the phenotype of cTnT-related cardiomyopathies in mouse hearts.Strong cross-bridges potentiate the Ca(2+) affinity changes produced by hypertrophic cardiomyopathy cardiac troponin C mutants in myofilaments: a fast kinetic approach.Abnormal heart rate regulation in murine hearts with familial hypertrophic cardiomyopathy-related cardiac troponin T mutationsCardiac troponin I Pro82Ser variant induces diastolic dysfunction, blunts β-adrenergic response, and impairs myofilament cooperativityElectrocardiographic Characterization of Cardiac Hypertrophy in Mice that Overexpress the ErbB2 Receptor Tyrosine Kinase.In Vivo Analysis of Troponin C Knock-In (A8V) Mice: Evidence that TNNC1 Is a Hypertrophic Cardiomyopathy Susceptibility GeneADP-stimulated contraction: A predictor of thin-filament activation in cardiac disease.Analysis of the molecular pathogenesis of cardiomyopathy-causing cTnT mutants I79N, ΔE96, and ΔK210.Focal energy deprivation underlies arrhythmia susceptibility in mice with calcium-sensitized myofilaments.Delineation of Molecular Pathways Involved in Cardiomyopathies Caused by Troponin T MutationsAbnormal blood pressure response to exercise occurs more frequently in hypertrophic cardiomyopathy patients with the R92W troponin T mutation than in those with myosin mutations.Increased myofilament Ca2+-sensitivity and arrhythmia susceptibility.Inherited cardiomyopathies caused by troponin mutations.Murine Electrophysiological Models of Cardiac Arrhythmogenesis.Calcium Signaling and Cardiac Arrhythmias.Myofilament Ca sensitization increases cytosolic Ca binding affinity, alters intracellular Ca homeostasis, and causes pause-dependent Ca-triggered arrhythmia.Diltiazem prevents stress-induced contractile deficits in cardiomyocytes, but does not reverse the cardiomyopathy phenotype in Mybpc3-knock-in mice.Increase in tension-dependent ATP consumption induced by cardiac troponin T mutation.F110I and R278C troponin T mutations that cause familial hypertrophic cardiomyopathy affect muscle contraction in transgenic mice and reconstituted human cardiac fibers.Diltiazem treatment prevents diastolic heart failure in mice with familial hypertrophic cardiomyopathy.Troponin T and beta-myosin mutations have distinct cardiac functional effects in hypertrophic cardiomyopathy patients without hypertrophy.Pathogenesis of depression- and anxiety-like behavior in an animal model of hypertrophic cardiomyopathy.Epac-induced ryanodine receptor type 2 activation inhibits sodium currents in atrial and ventricular murine cardiomyocytes.Cardiomyocyte ionic currents in intact young and aged murine Pgc-1β-/- atrial preparations.Ranolazine antagonizes catecholamine-induced dysfunction in isolated cardiomyocytes, but lacks long-term therapeutic effects in vivo in a mouse model of hypertrophic cardiomyopathy.Hypertrophic cardiomyopathy-linked mutation in troponin T causes myofibrillar disarray and pro-arrhythmic action potential changes in human iPSC cardiomyocytes.Simulation of the effects of moderate stimulation/inhibition of the β1-adrenergic signaling system and its components in mouse ventricular myocytes.Functional consequences of hypertrophic and dilated cardiomyopathy-causing mutations in alpha-tropomyosin.Mitochondrial Ca2+ Influx Contributes to Arrhythmic Risk in Nonischemic Cardiomyopathy.Heart angiotensin II-induced cardiomyocyte hypertrophy suppresses coronary angiogenesis and progresses diabetic cardiomyopathy.
P2860
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P2860
Inotropic stimulation induces cardiac dysfunction in transgenic mice expressing a troponin T (I79N) mutation linked to familial hypertrophic cardiomyopathy.
description
2000 nî lūn-bûn
@nan
2000年の論文
@ja
2000年学术文章
@wuu
2000年学术文章
@zh
2000年学术文章
@zh-cn
2000年学术文章
@zh-hans
2000年学术文章
@zh-my
2000年学术文章
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@zh-hant
name
Inotropic stimulation induces ...... l hypertrophic cardiomyopathy.
@en
Inotropic stimulation induces ...... c mice expressing a troponin T
@nl
type
label
Inotropic stimulation induces ...... l hypertrophic cardiomyopathy.
@en
Inotropic stimulation induces ...... c mice expressing a troponin T
@nl
prefLabel
Inotropic stimulation induces ...... l hypertrophic cardiomyopathy.
@en
Inotropic stimulation induces ...... c mice expressing a troponin T
@nl
P2093
P2860
P356
P1476
Inotropic stimulation induces ...... l hypertrophic cardiomyopathy.
@en
P2093
Housmans PR
Knollmann BC
Weissman NJ
de Freitas F
P2860
P304
10039-10048
P356
10.1074/JBC.M006745200
P407
P577
2000-12-11T00:00:00Z