Makoto Ishibashi

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: Results suggest that HES-1 normally controls the proper timing of neurogenesis and regulates neural tube morphogenesis.

TL;DR: Wnt7a and Wnt7b encode two Wnt ligands produced by the neuroepithelium of the developing CNS coincident with vascular invasion that directly target the vascular endothelium and that the CNS uses the canonical Wnt signaling pathway to promote formation and CNS-specific differentiation of the organ's vasculature.

TL;DR: Results show that persistent expression of HES‐1 severely perturbs neuronal and glial differentiation in the developing mammalian central nervous system.

TL;DR: The results suggest that MATH-1 may be a target of HES-1 and play a role in the differentiation of subsets of neural cells by activating E box-dependent transcription.