The regulatory programs governing skeletal muscle regeneration that are controlled by Klf5 in cooperation with MyoD and Mef2 provide a potential avenue for intervention into muscle regeneration through modulation of Klf5.

Actin-related protein 5 antagonizes the interaction of Pbx/Meis with myogenic regulatory factors such as MyoD and MyoG, which is involved in the recruitment of the BRG1-based switch/sucrose nonfermentable chromatin remodeling complex required for myogenic gene activation.

Genetic mouse models combined with single-cell RNA sequencing reveal the essential role of SRSF2 in directing MyoD progenitors to distinct skeletal muscle domains and controlling their differentiation through the regulation of targeted genes and alternative splicing during skeletal muscle development.

The myogenic lineage transcription factor, MYOD1, amplifies and works with the core clock factors to support a daily muscle gene expression program.

While current theories assume that mood is dominated by most recent experiences, computational modeling shows that mood is shaped by first experiences that carry a long-lasting overarching influence on mood.

Invasive electrophysiological recordings from the human brain reveal that different mood levels translate into different brain states that predispose subjects to make risky or safe decisions.

PASK phosphorylates Wdr5 to trigger epigenetic changes at lineage specifying promoters resulting in transcriptional derepression and differentiation of stem or progenitor cells.

Genetic and biochemical evidence shows that the basal transcription machinery of muscle cells invariably relies on TBP/TFIID because TBP2 is not expressed in muscle cells, and thus resolves a longstanding issue raised by previous conflicting data.

MYF5 and MYOD regulate rhabdomyosaroma growth and tumor-propagating potential, acting more than as passive markers retained from the target cell-of-origin during transformation.

Toxoplasma gondii formins have several non-overlapping roles including generating an apico-basal flux of F-actin that is controlled by phosphorylation and methylation and is essential for motility.