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The Importance of Intrinsically Disordered Segments of Cardiac Troponin in Modulating Function by Phosphorylation and Disease-Causing MutationsWhy Is there a Limit to the Changes in Myofilament Ca2+-Sensitivity Associated with Myopathy Causing Mutations?Investigations into the Sarcomeric Protein and Ca2+-Regulation Abnormalities Underlying Hypertrophic Cardiomyopathy in Cats (Felix catus).The dilated cardiomyopathy-causing mutation ACTC E361G in cardiac muscle myofibrils specifically abolishes modulation of Ca(2+) regulation by phosphorylation of troponin IOBSCN Mutations Associated with Dilated Cardiomyopathy and Haploinsufficiency.Muscle weakness in TPM3-myopathy is due to reduced Ca2+-sensitivity and impaired acto-myosin cross-bridge cycling in slow fibres.A dilated cardiomyopathy mutation blunts adrenergic response and induces contractile dysfunction under chronic angiotensin II stressInstrumentation to study myofibril mechanics from static to artificial simulations of cardiac cycle.Myosin regulatory light chain (RLC) phosphorylation change as a modulator of cardiac muscle contraction in diseaseMyopathy-inducing mutation H40Y in ACTA1 hampers actin filament structure and functionMutations in troponin T associated with Hypertrophic Cardiomyopathy increase Ca(2+)-sensitivity and suppress the modulation of Ca(2+)-sensitivity by troponin I phosphorylation.A post-MI power struggle: adaptations in cardiac power occur at the sarcomere level alongside MyBP-C and RLC phosphorylationTPM3 deletions cause a hypercontractile congenital muscle stiffness phenotype.Obscurin variants and inherited cardiomyopathies.The Sydney Heart Bank: improving translational research while eliminating or reducing the use of animal models of human heart disease.'(De-)sensitization' vs. 'Uncoupling': what drives cardiomyopathies in the thin filament? Reply.Abnormal contractility in human heart myofibrils from patients with dilated cardiomyopathy due to mutations in TTN and contractile protein genes.Tropomyosin Must Interact Weakly with Actin to Effectively Regulate Thin Filament Function.Age- and strain-related aberrant Ca2+ release is associated with sudden cardiac death in the ACTC E99K mouse model of hypertrophic cardiomyopathy.Troponin structure: its modulation by Ca(2+) and phosphorylation studied by molecular dynamics simulations.Molecular Defects in Cardiac Myofilament Ca2+-Regulation Due to Cardiomyopathy-Linked Mutations Can Be Reversed by Small Molecules Binding to Troponin.Isogenic Pairs of hiPSC-CMs with Hypertrophic Cardiomyopathy/LVNC-Associated ACTC1 E99K Mutation Unveil Differential Functional DeficitsThe Molecular Mechanisms of Mutations in Actin and Myosin that Cause Inherited Myopathy.Temperature-sensitive sarcomeric protein post-translational modifications revealed by top-down proteomicsThe homozygous K280N troponin T mutation alters cross-bridge kinetics and energetics in human HCMThe European Muscle Conference 2019 Special IssueTroponin structure and function: a view of recent progressPressure Overload Is Associated With Low Levels of Troponin I and Myosin Binding Protein C Phosphorylation in the Hearts of Patients With Aortic StenosisSmall molecule studies: the fourth wave of muscle research
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description
investigador
@es
researcher
@en
wetenschapper
@nl
name
Steven B Marston
@en
Steven B Marston
@nl
type
label
Steven B Marston
@en
Steven B Marston
@nl
prefLabel
Steven B Marston
@en
Steven B Marston
@nl
P31
P496
0000-0001-6054-6070