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.

Proinsulin misfolding, an established cause of diabetes in patients with INS gene mutations, is now observed in normal human pancreatic islets, and rodents with genetic predisposition to type 2 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.

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

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.

The endoplasmic reticulum (ER) uses ER tubules and specific ER autophagy machinery to prevent toxic, dominant-interfering, disease-causing, mutant proteins from entering the secretory pathway.

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.

ATP enters the endoplasmic reticulum (ER) lumen through an SLC35B1/AXER-dependentCaATiER mechanism, and ATP usage in the ER renders 'anti-Warburg' effect by increasing ATP regeneration from OxPhos while decreasing glycolysis.

A unique form of regulation has been observed in the unfolded protein response of S. pombe, along with a novel mechanism of post-transcriptional mRNA processing.

Integrated stress response-induced expression of ATF4 and its transactivation of SOX9 causes aberrant chondrocyte differentiation and skeletal defects which can be alleviated by modulating initiation-factor eIF2α phosphorylation translation control.