51 results found
    1. Human Biology and 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. Cell Biology
    2. Human Biology and Medicine

    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. Human Biology and 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. Cell Biology
    2. Human Biology and Medicine

    Muscle Contraction: Too much of a good thing

    H Lee Sweeney
    A mutation that causes heart disease in humans increases the number of active myosin heads during contraction in the muscles of fruit flies, leading to the progressive dysfunction of the flight muscles and heart tube.
    Insight
    Available as:
    • HTML
    • PDF
    1. Cell Biology
    2. Developmental Biology

    The Calcineurin-FoxO-MuRF1 signaling pathway regulates myofibril integrity in cardiomyocytes

    Hirohito Shimizu et al.
    Calcium overload in cardiomyocytes disrupts sarcomere integrity, by stimulating transcriptional upregulation of the E3 ubiquitin ligase MuRF1.
    1. Cell Biology
    2. Developmental Biology

    Genetic screen in Drosophila muscle identifies autophagy-mediated T-tubule remodeling and a Rab2 role in autophagy

    Naonobu Fujita et al.
    Analyses of a developmentally regulated Drosophila myofiber remodeling program provide insight into induced autophagy required for T-tubule membrane reorganization, and uncover a conserved Rab2 role in autophagosome-lysosome fusion.
    1. Human Biology and Medicine
    2. Structural Biology and Molecular Biophysics

    A calcium transport mechanism for atrial fibrillation in Tbx5-mutant mice

    Wenli Dai et al.
    TBX5-loss associated cardiomyocyte ectopy and atrial fibrillation is prevented by augmentation of SERCA2 activity, establishing a mechanism underlying the genetic basis for a Ca2+-dependent pathway for AF risk.

Refine your results by:

Type
Research categories