Exploring how proliferation and maturation of beta-cells can be impaired after birth will shed light on the origins of various forms of diabetes.

Mutations causing proinsulin misfolding trigger unfolded protein response and lead to impaired proliferation and reduced mTORC1 signalling of developing beta-cells in a patient-derived induced pluripotent stem cell disease model.

A previously undescribed protein produced by certain resident intestinal bacteria induces zebrafish pancreatic beta cell expansion.

During aging, the pancreatic endocrine islets undergo chronic inflammation, which is associated with a reduced capacity for self-renewal of the insulin-producing beta-cells in zebrafish.

Differentiation of CD4 T cells into CD4 T follicular helper cells during viral infection in mice is promoted by tumor growth factor beta.

A Na,K-ATPase beta subunit can suppress basal cell carcinogenesis either via its osmoregulatory function to avoid hypotonic stress, or by promoting epithelial polarity and adhesiveness of basal keratinocytes from the overlying outer layer.

mTORC1 inhibition by perinatal ER stress induces beta-cell growth arrest with subsequent development of diabetes.

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