Po Zhao

TL;DR: These experiments reveal that AMPK, Nampt, and SIRT1 are the molecular components of a functional signaling pathway that allows skeletal muscle cells to sense and react to nutrient availability.

TL;DR: Results indicate that Sir2 regulates muscle gene expression and differentiation by possibly functioning as a redox sensor in response to exercise, food intake, and starvation, Sir2 may sense modifications of the redox state and promptly modulate gene expression.

TL;DR: It is hypothesize that the abnormal Ca2+ influx in dystrophin- and α-sarcoglycan–deficient myofibers leads to altered developmental programming of developing and regenerating my ofibers, and that primary genetic defects can be identified by a reduction in the corresponding RNA.

TL;DR: A transcriptional model for downstream consequences of LMNA and emerin mutations is developed and it is proposed that key interactions between the nuclear envelope and Rb and MyoD fail in EDMD at the point of myoblast exit from the cell cycle, leading to poorly coordinated phosphorylation and acetylation steps.

TL;DR: Reducing the levels of p68/p72 proteins impaired recruitment of the TATA binding protein TBP; RNA polymerase II; and the catalytic subunit of the ATPase SWI/SNF complex, Brg-1, and hindered chromatin remodeling.