The fusion of astronomy and cellular cardiology reveals the 3D arrangement and the firing reliability of active excitation-contraction coupling sites in beating cardiac myocytes.

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.

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

A multi-species chemical screening platform reveals a conserved role for p38 inhibition in modulating ryanodine receptor-related phenotypes and is adaptable to a range of neuromuscular disorders.

An integrative model of coordinated crawling in fruit fly maggots links neuromuscular dynamics to body-substrate mechanics in the presence of proprioceptive feedback.

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.

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.

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