Rafael Jesus Fernandez, Zachary JG Gardner ... F Brad Johnson
Telomere dysfunction in iPSC-derived type II alveolar epithelial cells causes senescence and gene expression changes including Wnt-related changes that GSK3 inhibition can rescue, providing insight into pulmonary fibrosis pathogenesis.
Sox2 transcription is not correlated with spatial proximity of its essential regulatory enhancer in embryonic stem cells, suggesting gene transcription is not limited to periods of direct enhancer-promoter contact.
Sophie M Morgani, Jie Su ... Anna-Katerina Hadjantonakis
Loss of the transcription factor Rreb1 results perturbs epithelial architecture during mouse development resulting in invasive cell behaviors, severe cardiovascular defects, and embryonic lethality.
A thorough insight into the previously unrecognised role of a critical developmental regulator known as TBXT in influencing the specification of human trunk neural crest cells, the presumed precursors of the childhood tumour neuroblastoma.
The signaling requirements to decouple proliferation of pancreatic progenitors from differentiation were elucidated and employed for the reproducible expansion, under GMP-compliant conditions, of pancreatic progenitors derived from different human pluripotent stem cell lines.
Romaric Bouveret, Ashley J Waardenberg ... Richard P Harvey
Some NKX2-5 mutations that cause congenital heart disease retain transcriptional activity and can bind to many off-target genes, in part through their interactions with cofactors.
The cooperative action of PAF15 deubiquitylation by USP7 and its dissociation from chromatin by ATAD5 regulates proper PAF15Ub2 signaling termination, which is important for replication and maintenance of DNA methylation.
Alexandre P Thiery, Ariane SI Standing ... Gareth J Fraser
The development of diverse tooth shapes among vertebrates, from sharks to mammals, is a highly conserved process, utilising a similar dental signalling centre for more than 400 million years.
Rolando Ruiz-Vega, Chi-Fen Chen ... Arthur D Lander
Spontaneous growth arrest of transformed melanocytes (resulting in benign “moles”) does not result from cell-autonomous oncogene-induced senescence, but can be explained by collective mechanisms used in normal tissue size control.