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

The heart is able to sense and adaptively respond to environmental changes due to cardiac injury through flow-mediated mechanisms that regulate cardiomyocyte reprogramming and regeneration.

Making a link between deletion of transcription cis-regulatory elements by CrispR/Cas9, obtention of mutants with single muscle morphology defects and their impact on locomotion.

Lactate in pancreatic cancer micro-environment can lead to TET enzyme activation and loss of DNA methylation seen in cancer associated fibroblasts.

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.

Direct reprogramming of somatic cells to an inner ear sensory hair cell-like state provides an experimental platform to identify causes and treatments for hair cell loss and hearing deficits.

An in vitro chemical screen with single-cell sequencing output leads to the identification of Metformin as an in vivo enhancer of Muller glia to neuron reprogramming in mice.

DNA methylation deposition is dependent on the presence of H3K4me3 and H3K36me3 histone marks.

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

Cells from vertebrate and invertebrate model systems can be reprogrammed into stem-like cells using mouse genes.