Detailed studies of excitation contraction coupling allowed determination of quantitative relationships between resting potential, generation of action potentials, conduction of action potentials, and generation of Ca²⁺ transients in individual mouse skeletal muscle fibers.

Genetic or pharmacological suppression of lipid peroxidation pathway protects skeletal muscle from disuse-induced atrophy and weakness in young and old mice.

The Ryanodine receptor type 1 calcium channels play a critical role in age-related muscle function loss.

Vertebrate superfast muscles employ similar excitation–contraction strategies but distinct myosin heavy chain genes to allow superfast performance, revealing a maximum speed that cannot be overcome without sacrificing neural control.

Genetic reduction of Numb or Numb/Nubl is linked to deterioration of the Septin cytoskeleton and suggests cytoskeletal abnormalities are the consequences of and contribute to age-related changes in skeletal muscle.

Global proteomic and acetylomic analyses reveal how skeletal muscle adapts to high-intensity interval training including adaptations to processes regulating metabolism and contraction.

Characterization of Ca²⁺ selectivity and non-conductance mechanism induced by pore mutation N617D in the skeletal muscle DHPR.

Quantitative proteomic analysis shows that recessive Ryr1 mutations not only decrease the content of RyR1 protein in muscle, but also affect the content of many other proteins involved in a variety of biological processes.

iMyoblasts, a novel iPS-derived PAX3 muscle stem cell for gene editing, muscle engraftment, and stem cell therapeutics to treat muscle injury and muscular dystrophies.

Caveolae and Bin1 form tubulation platforms.