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.

Variation in efficiency, speed and path during transdifferentiation and reprogramming originates from two pre-B cell subpopulations with reciprocal propensity towards each fate conversion.

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.

Induced neuronal cells acquire epigenomic signatures specific to matured neurons.

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

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