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

Cells from the human pancreatic duct can be grown in culture and triggered to become insulin-producing cells, which could potentially be transplanted into patients with diabetes.

The regulation of beta cell induction requires combined hierarchical and combinatorial transcriptional networks.

Intercellular communication is critical for organ function, and the role of innervation in mediating this communication is of relevance to many fields, including developmental biology, neuroendocrinology, and disease pathophysiology.

Analysis of epigenome maps from human pancreatic progenitors and functional validation in zebrafish identify LAMA1 and CRB2 as type 2 diabetes risk-associated genes with roles in pancreatic development.

ECM-Itgb1 signaling and cell-cell adhesion are pivotal and coordinate together to regulate pancreatic islet aggregation, architecture, and functional maturation during development.

A set of cell surface markers reconstruct human pancreatic differentiation and enable the segregation of pancreatic functions into specific populations.

Genetic analyses revealed the remarkable plasticity of mesodermal cells to differentiate across the germ layers to form insulin-producing β-cells, which are normally of endodermal origin.

Loss of YAP1/TAZ expression in the pancreatic endocrine compartment is not a passive consequence of endocrine specification, rather, Hippo pathway-mediated inhibition of YAP1/TAZ in endocrine progenitors is a prerequisite for endocrine specification and differentiation.

Ribosome profiling and loss-of-function during human ESC pancreatic differentiation reveal abundant lncRNA translation and an essential role for translated LINC00261 in beta cell differentiation, likely through a trans-regulatory, microprotein-independent mechanism.