99 results found
    1. Cell Biology

    Prolonged cross-bridge binding triggers muscle dysfunction in a Drosophila model of myosin-based hypertrophic cardiomyopathy

    William A Kronert et al.
    Integrative analysis of a Drosophila model of hypertrophic cardiomyopathy demonstrates that prolonged binding of the myosin cross-bridge to actin is a root cause of the disorder.
    1. Medicine

    Effects of myosin variants on interacting-heads motif explain distinct hypertrophic and dilated cardiomyopathy phenotypes

    Lorenzo Alamo et al.
    Mapping the locations of hypertrophic cardiomyopathy gene variants onto the three-dimensional structures of contractile proteins revealed that these disrupt protein interactions are critical for normal cardiac relaxation and efficient energy usage.
    1. Cell Biology

    The DWORF micropeptide enhances contractility and prevents heart failure in a mouse model of dilated cardiomyopathy

    Catherine A Makarewich et al.
    Cardiac-specific overexpression of a recently discovered micropeptide, DWORF, enhances calcium cycling and contractility in the heart and rescues the heart failure phenotype of a genetic mouse model of dilated cardiomyopathy.
    1. Medicine

    Loss of the melanocortin-4 receptor in mice causes dilated cardiomyopathy

    Michael J Litt et al.
    The melanocortin-4 receptor knockout mouse exhibits a cardiomyopathy syndrome, which raises concerns about cardiovascular function in patients with the similar loss of function mutations, and perhaps even in the 1 in 1500 patients with heterozygous loss of the gene.
    1. Genetics and Genomics

    An internal promoter underlies the difference in disease severity between N- and C-terminal truncation mutations of Titin in zebrafish

    Jun Zou et al.
    The newly discovered Titin internal promoter may explain why the severity of dilated cardiomyopathy in patients with truncating mutations in Titin varies dramatically depending on position of the mutation.
    1. Biochemistry and Chemical Biology
    2. Structural Biology and Molecular Biophysics

    Myosin with hypertrophic cardiac mutation R712L has a decreased working stroke which is rescued by omecamtiv mecarbil

    Aaron Snoberger et al.
    Mechanochemical defects of a β-cardiac myosin mutation that results in severe hypertrophic cardiomyopathy are reported and the heart failure drug omecamtiv mecarbil rescues these defects.
    1. Developmental Biology
    2. Genetics and Genomics

    Cardiac pathologies in mouse loss of imprinting models are due to misexpression of H19 long noncoding RNA

    Ki-Sun Park et al.
    Maternal loss of imprinting at the Igf2/H19 locus reduces expression of H19 lncRNA and thereby leads to progressive cardiac pathologies in a mouse Beckwith–Wiedemann syndrome model.
    1. Developmental Biology
    2. Chromosomes and Gene Expression

    EED orchestration of heart maturation through interaction with HDACs is H3K27me3-independent

    Shanshan Ai et al.
    During heart maturation, embryonic ectoderm development as a chromatin remodeler triggers transcriptional silencing, while H3K27me3 is a passenger that is not sufficient for gene silencing.
    1. Cell Biology
    2. Computational and Systems Biology

    Development, calibration, and validation of a novel human ventricular myocyte model in health, disease, and drug block

    Jakub Tomek et al.
    A computer model of human cardiomyocyte was produced and validated on independent datasets, overcoming shortcomings of its predecessors, also yielding broadly relevant insights and results on major ionic currents.
    1. Biochemistry and Chemical Biology
    2. Structural Biology and Molecular Biophysics

    To lie or not to lie: Super-relaxing with myosins

    Suman Nag, Darshan V Trivedi
    A perspective of the energy-sparing super-relaxed state of myosin and its evolutionary role in modulating skeletal and cardiac muscle power under different physiological and pathophysiological perturbations.

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