Enhanced active cross-bridges during diastole: molecular pathogenesis of tropomyosin's HCM mutations - Wikidata - awgldk - TriplyDB

Enhanced active cross-bridges during diastole: molecular pathogenesis of tropomyosin's HCM mutations

Enhanced active cross-bridges during diastole: molecular pathogenesis of tropomyosin's HCM mutations

http://www.wikidata.org/entity/Q34568089

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A Drosophila melanogaster model of diastolic dysfunction and cardiomyopathy based on impaired troponin-T function.Phosphorylation of cMyBP-C affects contractile mechanisms in a site-specific manner Persistence length of human cardiac α-tropomyosin measured by single molecule direct probe microscopy.DCM-related tropomyosin mutants E40K/E54K over-inhibit the actomyosin interaction and lead to a decrease in the number of cycling cross-bridges.Mechanistic heterogeneity in contractile properties of α-tropomyosin (TPM1) mutants associated with inherited cardiomyopathies.Multi-scale computational models of familial hypertrophic cardiomyopathy: genotype to phenotype.Structural and functional aspects of the myosin essential light chain in cardiac muscle contraction.Facilitated cross-bridge interactions with thin filaments by familial hypertrophic cardiomyopathy mutations in α-tropomyosin.Micromechanical thermal assays of Ca2+-regulated thin-filament function and modulation by hypertrophic cardiomyopathy mutants of human cardiac troponin Detection of target ssDNA using a microfabricated Hall magnetometer with correlated optical readout.Fluorescent Protein-Based Ca2+ Sensor Reveals Global, Divalent Cation-Dependent Conformational Changes in Cardiac Troponin C Congenital myopathy-causing tropomyosin mutations induce thin filament dysfunction via distinct physiological mechanisms.Analysis of the molecular pathogenesis of cardiomyopathy-causing cTnT mutants I79N, ΔE96, and ΔK210.Slowed Dynamics of Thin Filament Regulatory Units Reduces Ca(2+)-Sensitivity of Cardiac Biomechanical Function.The functional significance of the last 5 residues of the C-terminus of cardiac troponin I.Diversity and similarity of motor function and cross-bridge kinetics in papillary muscles of transgenic mice carrying myosin regulatory light chain mutations D166V and R58Q Predicting Effects of Tropomyosin Mutations on Cardiac Muscle Contraction through Myofilament Modeling.Transmission of stability information through the N-domain of tropomyosin is interrupted by a stabilizing mutation (A109L) in the hydrophobic core of the stability control region (residues 97-118).Effect of N-Terminal Extension of Cardiac Troponin I on the Ca(2+) Regulation of ATP Binding and ADP Dissociation of Myosin II in Native Cardiac Myofibrils.The 3-state model of muscle regulation revisited: is a fourth state involved?Thin filament-reconstituted skinned muscle fibers for the study of muscle physiology.Interpreting genetic effects through models of cardiac electromechanics.A study of tropomyosin's role in cardiac function and disease using thin-filament reconstituted myocardium.Nuclear tropomyosin and troponin in striated muscle: new roles in a new locale?Alpha-tropomyosin mutations in inherited cardiomyopathies.The myosin-activated thin filament regulatory state, M⁻-open: a link to hypertrophic cardiomyopathy (HCM).Role of multimodality cardiac imaging in the management of patients with hypertrophic cardiomyopathy: an expert consensus of the European Association of Cardiovascular Imaging Endorsed by the Saudi Heart Association.Using baculovirus/insect cell expressed recombinant actin to study the molecular pathogenesis of HCM caused by actin mutation A331P Pathogenesis of Hypertrophic Cardiomyopathy is Mutation Rather Than Disease Specific: A Comparison of the Cardiac Troponin T E163R and R92Q Mouse Models.Long-range effects of familial hypertrophic cardiomyopathy mutations E180G and D175N on the properties of tropomyosin Tropomyosin flexural rigidity and single ca(2+) regulatory unit dynamics: implications for cooperative regulation of cardiac muscle contraction and cardiomyocyte hypertrophy.Familial hypertrophic cardiomyopathy related E180G mutation increases flexibility of human cardiac α-tropomyosin.α-Tropomyosin with a D175N or E180G mutation in only one chain differs from tropomyosin with mutations in both chains.Effect of Cardiomyopathic Mutations in Tropomyosin on Calcium Regulation of the Actin-Myosin Interaction in Skeletal Muscle.

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Enhanced active cross-bridges during diastole: molecular pathogenesis of tropomyosin's HCM mutations

http://www.wikidata.org/entity/Q34568089

description

2011 nî lūn-bûn

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2011 թուականի Փետրուարին հրատարակուած գիտական յօդուած

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2011 թվականի փետրվարին հրատարակված գիտական հոդված

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2011年の論文

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Enhanced active cross-bridges ...... of tropomyosin's HCM mutations

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Enhanced active cross-bridges ...... of tropomyosin's HCM mutations

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Enhanced active cross-bridges ...... of tropomyosin's HCM mutations

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Enhanced active cross-bridges ...... of tropomyosin's HCM mutations

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Enhanced active cross-bridges ...... of tropomyosin's HCM mutations

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Enhanced active cross-bridges ...... of tropomyosin's HCM mutations

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Enhanced active cross-bridges ...... of tropomyosin's HCM mutations

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Enhanced active cross-bridges ...... of tropomyosin's HCM mutations

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Enhanced active cross-bridges ...... of tropomyosin's HCM mutations

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J.BPJ.2011.01.001

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Enhanced active cross-bridges ...... of tropomyosin's HCM mutations

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Adam Weis

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Aya K Takeda

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Fan Bai

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P2860

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

Alpha-tropomyosin and cardiac troponin T mutations cause familial hypertrophic cardiomyopathy: a disease of the sarcomere

Single-molecule mechanics of R403Q cardiac myosin isolated from the mouse model of familial hypertrophic cardiomyopathy

Conformational parameters for amino acids in helical, beta-sheet, and random coil regions calculated from proteins

Regulation of the interaction between actin and myosin subfragment 1: evidence for three states of the thin filament

Mutations in the gene for cardiac myosin-binding protein C and late-onset familial hypertrophic cardiomyopathy

Shared genetic causes of cardiac hypertrophy in children and adults

Genotype-phenotype relationships involving hypertrophic cardiomyopathy-associated mutations in titin, muscle LIM protein, and telethonin

Differential cross-bridge kinetics of FHC myosin mutations R403Q and R453C in heterozygous mouse myocardium

Autocrine release of angiotensin II mediates stretch-induced hypertrophy of cardiac myocytes in vitro

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