The major protein disulfide isomerase family member, PDIA1, is essential in beta cells of mice fed a high-fat diet to maintain glucose homeostasis, proinsulin maturation and organelle integrity.

HID-1 is a novel player mediating homotypic fusion of immature secretory granules.

The mechanism identified here that mediates olanzapine-induced b-cell dysfunction should be considered, along with weight gain, in mitigating adverse side effects when patients with schizophrenia are prescribed olanzapine.

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.

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

Insulin secreting cells harbor distinct subpopulations of insulin granules and loss of one or the other correlates strongly with secretory deficiencies characterizing type-1 or type-2 diabetes.

Death receptor 5 can directly sense misfolded proteins downstream of the endoplasmic reticulum to provide a quality control mechanism that executes apoptosis and prevents further production of misfolded proteins.

High glucose levels promote CTSL maturation and translocation from the endoplasmic reticulum to the lysosome via the ER-Golgi-lysosome axis.

The first human TANGO1-associated syndromal disease manifests as impaired collagen secretion, highlighting the importance of TANGO1 in human pathophysiology.