Jacob Hald

TL;DR: It is shown that mice deficient in Hes1 (encoding Hes-1) display severe pancreatic hypoplasia caused by depletion of pancreatic epithelial precursors due to accelerated differentiation of post-mitotic endocrine cells expressing glucagon, and upregulation of several bHLH components is associated with precocious and excessive differentiation of multiple endocrine cell types in the developing stomach and gut, showing that Hes- 1 operates as a general negative regulator of endodermal endocrine differentiation.

TL;DR: How this global analysis of the developing pancreas confirms and extends previous studies is discussed, and it is envisaged that this type of analysis can be instrumental for evaluating mutant phenotypes in the future.

TL;DR: Investigation of the effect of expressing a constitutively active form of the Notch1 receptor (Notch1(ICD) in the developing pancreas using the pdx1 promoter reveals a disorganized pancreatic epithelium with reduced numbers of endocrine cells, confirming a repressive activity of NotCh1 upon the early differentiation program.

TL;DR: HNF6 and Sox9 are new biomarkers of ADM and constitute candidate targets for preventive treatment in cases when ADM may lead to cancer, and shows that ectopic activation of transcription factors may underlie metaplastic processes occurring in other organs.

TL;DR: Overall, the EndoC-βH1 cells strongly resemble human islet beta cells in terms of glucose and incretin stimulated insulin secretion capabilities and was successfully used as a screening platform for identification of novel anti-diabetic drug candidates.