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

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

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.

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

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.

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.

The epigenetic regulation of adult muscle stem cell fate by lnc-Rewind relies on the RNA-mediated recruitment of G9a methyltransferase on the Wnt7b genomic locus.

Cellular and molecular analyses reveal how Myogenin controls muscle stem cell quiescence and growth of adult muscle fibres.

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.

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.