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.

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.

Acute lymphoblastic and myeloblastic leukemias activate lymphotoxin beta receptor in mesenchymal stem cells in the bone marrow to turn off interleukin-7 production and lymphopoiesis and gain competitive advantage.

One-step Isolation and Lysis (OIL) PCR offers a robust, versatile, accessible, and high-throughput method for linking mobile DNA with bacterial hosts in natural microbial communities.

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

The secretion of insulin from the pancreas relies on both gap junctions and subpopulations of beta cells with specific intrinsic properties.

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

In vitro culture of brain endothelial cells leads to a rapid loss of the blood-brain barrier transcriptional and accessible chromatin landscapes that is resistant to the effects of beta-catenin stabilization.

Pancreatic α and β cells have different cell autonomous signatures; this explains why α but not β cells can clear infections by potentially diabetogenic viruses.