In the present seminar, I will summarize our findings concerning the role of Srf
in myofibers to control muscle mass and I will present recent data identifying Srf as a master regulator of muscle stem cell fusion and demonstrating the implication of F - actin architecture in this process.
Osteocalcin signaling
in myofibers is necessary and sufficient for optimum adaptation to exercise.
Not exact matches
Studies had shown that
myofibers, the cells making up these muscles, were larger and greater
in number — producing a more powerful bite.
Although reactive oxygen species can damage cells when produced
in high amounts, according to a study published online Sept. 5, 2017 by Science Signaling and featured on the journal's cover, these oxidative species are crucial signals that start the process of repairing
myofiber.
We investigated the role of Srf
in two cellular compartments of mouse skeletal muscle (
myofibers and adult muscle stem cells) upon different perturbation of muscle homeostasis (hypertrophy, atrophy, regeneration).
We previously demonstrated that numerous Wnt molecules are secreted
in the local milieu during regeneration and showed that MuSC self - renewal is
in part controlled by non-canonical Wnt7a / PCP signals sent by the regenerating
myofibers.
Effect of the different experimental conditions on the glycogen, intracellular glucose, and G6P content
in cultures of human
myofibers.
Effect of preculturing human satellite cell cultures
in increasing concentrations of insulin on the basal and insulin - stimulated glucose transport activity
in cultures of human
myofibers.
Potent
myofiber hypertrophy during resistance training
in humans is associated with satellite cell - mediated myonuclear addition: a cluster analysis.
Translational signaling responses preceding resistance training - mediated
myofiber hypertrophy
in young and old humans.
Efficacy of 3 days / wk resistance training on
myofiber hypertrophy and myogenic mechanisms
in young vs. older adults
Myofiber size was appropriate
in all muscles evaluated and no specific abnormalities were identified, making a congenital myopathy unlikely.