Associated Papers
Accurate affinity models for SH2 domains from peptide binding assays and free-energy regression.
Gagoski D et al.
Protein Science : a Publication of the Protein Society, 2025
Experimental Models of Hypertrophic Cardiomyopathy: A Systematic Review.
van den Dolder FW et al.
Jacc. Basic to Translational Science, 2025
Accurate sequence-to-affinity models for SH2 domains from multi-round peptide binding assays coupled with free-energy regression.
Gagoski D et al.
Biorxiv : the Preprint Server for Biology, 2025
Identification of a novel likely pathogenic TPM1 variant linked to hypertrophic cardiomyopathy in a family with sudden cardiac death.
Azimi A et al.
Esc Heart Failure, 2024
Human Exome Sequencing and Prospects for Predictive Medicine: Analysis of International Data and Own Experience.
Glotov OS et al.
Journal of Personalized Medicine, 2023
Novel Mutation Glu98Lys in Cardiac Tropomyosin Alters Its Structure and Impairs Myocardial Relaxation.
Matyushenko AM et al.
International Journal of Molecular Sciences, 2023
Thin filament cardiomyopathies: A review of genetics, disease mechanisms, and emerging therapeutics.
Keyt LK et al.
Frontiers in Cardiovascular Medicine, 2022
Cardiomyocyte Dysfunction in Inherited Cardiomyopathies.
Hassoun R et al.
International Journal of Molecular Sciences, 2021
Advanced pathological study for definite diagnosis of mitochondrial cardiomyopathy.
Takeda A et al.
Journal of Clinical Pathology, 2020
Molecular Mechanisms of Pathologies of Skeletal and Cardiac Muscles Caused by Point Mutations in the Tropomyosin Genes.
Matyushenko AM et al.
Biochemistry. Biokhimiia, 2020
Evaluating the Clinical Validity of Hypertrophic Cardiomyopathy Genes.
Ingles J et al.
Circulation. Genomic and Precision Medicine, 2019
Sarcomere gene variants act as a genetic trigger underlying the development of left ventricular noncompaction.
Takasaki A et al.
Pediatric Research, 2018
Coverage and diagnostic yield of Whole Exome Sequencing for the Evaluation of Cases with Dilated and Hypertrophic Cardiomyopathy.
Mak TSH et al.
Scientific Reports, 2018
Late Gadolinium Enhancement for Prediction of Mutation-Positive Hypertrophic Cardiomyopathy on the Basis of Panel-Wide Sequencing.
Teramoto R et al.
Circulation Journal : Official Journal of the Japanese Circulation Society, 2018
Investigating the effects of tropomyosin mutations on its flexibility and interactions with filamentous actin using molecular dynamics simulation.
Zheng W et al.
Journal of Muscle Research and Cell Motility, 2016
Why Is there a Limit to the Changes in Myofilament Ca2+-Sensitivity Associated with Myopathy Causing Mutations?
Marston SB
Frontiers in Physiology, 2016
Primary prevention of sudden cardiac death in a low-risk child with familial hypertrophic cardiomyopathy: the role of cardiac magnetic resonance imaging.
Yamazawa H et al.
Clinical Research in Cardiology : Official Journal of the German Cardiac Society, 2014
A study of tropomyosin's role in cardiac function and disease using thin-filament reconstituted myocardium.
Bai F et al.
Journal of Muscle Research and Cell Motility, 2013
Alpha-tropomyosin mutations in inherited cardiomyopathies.
Redwood C et al.
Journal of Muscle Research and Cell Motility, 2013
Integrative structural modelling of the cardiac thin filament: energetics at the interface and conservation patterns reveal a spotlight on period 2 of tropomyosin.
Margaret Sunitha S et al.
Bioinformatics and Biology Insights, 2012
How do mutations in contractile proteins cause the primary familial cardiomyopathies?
Marston SB
Journal of Cardiovascular Translational Research, 2011
Thin filament mutations: developing an integrative approach to a complex disorder.
Tardiff JC
Circulation Research, 2011
Enhanced active cross-bridges during diastole: molecular pathogenesis of tropomyosin's HCM mutations.
Bai F et al.
Biophysical Journal, 2011
Identification of a novel TPM1 mutation in a family with left ventricular noncompaction and sudden death.
Chang B et al.
Molecular Genetics and Metabolism, 2011
Molecular and functional characterization of a novel cardiac-specific human tropomyosin isoform.
Rajan S et al.
Circulation, 2010
An internal domain of beta-tropomyosin increases myofilament Ca(2+) sensitivity.
Jagatheesan G et al.
American Journal of Physiology. Heart and Circulatory Physiology, 2009
Defective regulation of contractile function in muscle fibres carrying an E41K beta-tropomyosin mutation.
Ochala J et al.
The Journal of Physiology, 2008
Rescue of tropomyosin-induced familial hypertrophic cardiomyopathy mice by transgenesis.
Jagatheesan G et al.
American Journal of Physiology. Heart and Circulatory Physiology, 2007
Dilated cardiomyopathy mutant tropomyosin mice develop cardiac dysfunction with significantly decreased fractional shortening and myofilament calcium sensitivity.
Rajan S et al.
Circulation Research, 2007
The effect of mutations in alpha-tropomyosin (E40K and E54K) that cause familial dilated cardiomyopathy on the regulatory mechanism of cardiac muscle thin filaments.
Mirza M et al.
The Journal of Biological Chemistry, 2007
The Delta 14 mutation of human cardiac troponin T enhances ATPase activity and alters the cooperative binding of S1-ADP to regulated actin.
Gafurov B et al.
Biochemistry, 2004
Congenital myopathies: diseases of the actin cytoskeleton.
Clarkson E et al.
The Journal of Pathology, 2004
Effects of cardiomyopathic mutations on the biochemical and biophysical properties of the human alpha-tropomyosin.
Hilario E et al.
European Journal of Biochemistry, 2004
Parvalbumin corrects slowed relaxation in adult cardiac myocytes expressing hypertrophic cardiomyopathy-linked alpha-tropomyosin mutations.
Coutu P et al.
Circulation Research, 2004
Cardiomyopathic tropomyosin mutations that increase thin filament Ca2+ sensitivity and tropomyosin N-domain flexibility.
Heller MJ et al.
The Journal of Biological Chemistry, 2003
Prevalence and spectrum of thin filament mutations in an outpatient referral population with hypertrophic cardiomyopathy.
Van Driest SL et al.
Circulation, 2003
The role of tropomyosin in the regulation of myocardial contraction and relaxation.
Wolska BM et al.
Pflugers Archiv : European Journal of Physiology, 2003
Variable clinical manifestation of a novel missense mutation in the alpha-tropomyosin (TPM1) gene in familial hypertrophic cardiomyopathy.
Jongbloed RJ et al.
Journal of the American College of Cardiology, 2003
Molecular mechanisms of inherited cardiomyopathies.
Fatkin D et al.
Physiological Reviews, 2002
Calcium, contractions, and tropomyosin Focus on "divergent abnormal muscle relaxation by hypertrophic cardiomyopathy and nemaline myopathy mutant tropomyosins".
Marston SB et al.
Physiological Genomics, 2002
Divergent abnormal muscle relaxation by hypertrophic cardiomyopathy and nemaline myopathy mutant tropomyosins.
Michele DE et al.
Physiological Genomics, 2002
Invited Review: pathophysiology of cardiac muscle contraction and relaxation as a result of alterations in thin filament regulation.
Hernandez OM et al.
Journal of Applied Physiology (bethesda, Md. : 1985), 2001
Hypertrophic cardiomyopathy caused by a novel alpha-tropomyosin mutation (V95A) is associated with mild cardiac phenotype, abnormal calcium binding to troponin, abnormal myosin cycling, and poor prognosis.
Karibe A et al.
Circulation, 2001
The molecular genetics of hypertrophic cardiomyopathy: prognostic implications.
Sorajja P et al.
Europace : European Pacing, Arrhythmias, and Cardiac Electrophysiology : Journal of the Working Groups on Cardiac Pacing, Arrhythmias, and Cardiac Cellular Electrophysiology of the European Society of Cardiology, 2000
Physiological consequences of tropomyosin mutations associated with cardiac and skeletal myopathies.
Michele DE et al.
Journal of Molecular Medicine (berlin, Germany), 2000
Direct, convergent hypersensitivity of calcium-activated force generation produced by hypertrophic cardiomyopathy mutant alpha-tropomyosins in adult cardiac myocytes.
Michele DE et al.
Nature Medicine, 1999
Mouse model of a familial hypertrophic cardiomyopathy mutation in alpha-tropomyosin manifests cardiac dysfunction.
Muthuchamy M et al.
Circulation Research, 1999
Clinical features of hypertrophic cardiomyopathy caused by mutation of a "hot spot" in the alpha-tropomyosin gene.
Coviello DA et al.
Journal of the American College of Cardiology, 1997