ATF4, the master regulator of transcription during the Integrated Stress Response (ISR), causes global changes in cysteine sulfhydration of proteins and this event causes cellular metabolic reprogramming.

The reconstruction of damaged structures during regeneration requires cell reprogramming mediated by the up regulation of the JNK pathway and the transient debilitation of the epigenetic control mechanism.

A technology allows rapid screening of vast numbers of transcriptional factor combinatorials on stem cell programming.

Increased Notch signaling enhances germ cell reprograming in C. elegans by antagonizing PRC2-mediated repression, which results in the activation of UTX-1 and other reprograming-promoting genes.

Spatial and temporal cues intersect, likely via enhancer-promoter looping, to turn on a master identity switch that in turn dictates natural lineage reprogramming with high efficiency and temporospatial precision.

During reprogramming of human fibroblasts to naïve iPSCs there is transient reactivation of transcripts with the characteristics of 8-cell-stage-embryos.

Combinations of transcription factors can convert pancreatic acinar cells into endocrine α-, β- and δ-cells in vivo.

The vertebrate testis-determining gene, Sox9, also controls adult testis maintenance in mammals, acting redundantly with its paralog Sox8.

The OSM-9 TRPV channel is differentially regulated due to developmental programming via modulation by TGF-β signaling, endogenous RNAi and chromatin remodeling pathways.

Hemodynamic forces regulate endothelial cell metabolism, which in turn regulates endothelial inflammation.