Ablation of the Cdkn1c cell cycle inhibitor leads to defective muscle stem cell dynamics and myogenic potential, while progressive cytoplasmic to nuclear cellular localization of the Cdkn1c protein regulates growth arrest.

Large flight muscle of Drosophila are made by the regulated amplification of a newly identified stem cell population.

Modulation of muscle stem cell redox state in culture both improves their amplification while maintaining a similar grafting potential as freshly isolated stem cells.

Building on previous work (Liu et al., 2015), it is shown that depletion or rescue of adult skeletal muscle stem cells is sufficient to induce or attenuate age-associated neuromuscular junction deterioration respectively.

Proliferating muscle stem cells in overloaded muscle require special molecular mechanisms that differ from well-known myogenic differentiation model.

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.

Myomaker is activated on muscle stem cells to promote their fusion with myofibers, which is essential for induction of pro-growth signaling pathways and physiological muscle hypertrophy.

A set of ex vivo and in vivo experiments, including genetic ablation and regeneration studies, identify a key regulatory function of SOXF factors in muscle stem cells in mice.

Ablation of canonical TGFβ signaling in muscle stem cells at any age is detrimental, and not beneficial, to effective skeletal muscle regeneration due to the promotion of premature fate commitment at the expense of progenitor amplification.

Rescue of DUX4-induced muscle pathology by the RET inhibitor Sunitinib reveals the therapeutic potential for treatment of Facioscapulohumeral muscular dystrophy using tyrosine kinase inhibitors.