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A mouse model of human muscle myopathy is used to provide mechanistic insight, identify possible biomarkers of disease, and suggest possible therapeutic strategies to alleviate muscle weakness.

Skeletal muscle stem cells play important roles in the regeneration of neuromuscular junctions, and so present new targets for therapies to treat neuromuscular decline observed in the context of aging and various neuromuscular diseases.

Novel components in the pathway from malignant hyperthermia to diabetes include promotion of a kinase that impedes glycogen synthesis, increased lysis of junctophilin1 and gene regulatory actions by a junctophilin fragment, surprisingly predicted to oppose the effects of elevated calcium.

Structural and functional analyses show that transverse tubule association with stacks of sarcoplasmic reticulum enhances Orai1-dependent Ca²⁺ entry to replenish Ca²⁺ stores, maintain Ca²⁺ release, and maximize force during exercise.

Transient Ca elevations of cytoplasmic calcium in cardiac myocytes profoundly activate cardiac Na/K pump activity in parallel with physical-chemical changes of the sarcolemma but without involvement of conventional signaling mechanisms.

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.

The two Drosophila titin homologs Sallimus and Projectin display a precise tandem arrangement in the sarcomere that may explain how sarcomere length is regulated outside of vertebrates.

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.

Depending upon the parameters used, neuromuscular stimulation can have beneficial or deleterious impacts on muscle structure and function in an animal model of Duchenne muscular dystrophy.

Maintenance of peripheral myonuclei patterning in skeletal myofibers is dependent on the regulation of microtubules dynamic and nuclei motion and is essential for proper neuromuscular junction integrity and mitochondria homeostasis.