Mitochondria undergo fragmentation in response to electron transport chain (ETC) poisons
and mitochondrial DNA–linked disease mutations, yet how these stimuli mechanistically …

Muscle contraction depends on release of Ca2+ from the sarcoplasmic reticulum (SR) and
reuptake by the Ca2+ adenosine triphosphatase SERCA. We discovered a putative muscle …

Many neuromuscular disorders can have a differential impact on a specific myofibre type,
forming the central premise of this review. The many different skeletal muscles in mammals …

Aberrant expression of the cardiac gap junction protein connexin-43 (Cx43) has been
suggested as playing a role in the development of cardiac disease in the mdx mouse model …

Amyotrophic lateral sclerosis (ALS) is an adult-onset disease characterized by the
progressive death of motoneurons and denervation of muscle fibers. To restore motor …

The development of the neuromuscular system, including muscle growth and intramuscular
neural development, in addition to central nervous system maturation, determines motor …

Gpr126/Adgrg6 is an adhesion G protein‐coupled receptor essential for Schwann cell (SC)
myelination with important contributions to repair after nerve crush injury. Despite critical …

Activation of the tropomyosin-related kinase receptor B (TrkB) by brain-derived neurotrophic
factor acutely regulates synaptic transmission at adult neuromuscular junctions (NMJs). The …

Triadin (Tdn) and Junctin (Jct) are structurally related transmembrane proteins thought to be
key mediators of structural and functional interactions between calsequestrin (CASQ) and …

Mutations in Cu/Zn superoxide dismutase (SOD1) are one of the genetic causes of
Amyotrophic Lateral Sclerosis (ALS). Although the primary symptom of ALS is muscle …