Diabetes, ER stress, IAPP, UPR(13)
1 GATA factors promote ER integrity, beta-cell survival, and contribute to type 1 diabetes risk.
2 High Glucose Exposure Promotes Activation of Protein Phosphatase 2A in Rodent Islets and INS-1 832/13 beta-Cells by Increasing the Posttranslational Carboxylmethylation of Its Catalytic Subunit.
3 Molecular Simulations Indicate Marked Differences in the Structure of Amylin Mutants, Correlated with Known Aggregation Propensity.
4 A crosstalk between p21 and UPR-induced transcription factor C/EBP homologous protein (CHOP) linked to type 2 diabetes.
5 Beta cell dysfunction due to increased ER stress in a stem cell model of Wolfram syndrome.
6 Restoration of the Unfolded Protein Response in Pancreatic beta Cells Protects Mice Against Type 1 Diabetes.
7 Resident macrophages mediate islet amyloid polypeptide-induced islet IL-1beta production and beta cell dysfunction.
8 Oleate rescues INS-1E beta-cells from palmitate-induced apoptosis by preventing activation of the unfolded protein response.
9 Insulin Secretion and Ca2+ Dynamics in beta-Cells Are Regulated by PERK (EIF2AK3) in Concert with Calcineurin.
10 Blockade of islet amyloid polypeptide fibrillation and cytotoxicity by the secretory chaperones 7B2 and proSAAS.
11 Glucotoxic conditions induce endoplasmic reticulum stress to cause caspase 3 mediated lamin B degradation in pancreatic beta-cells: protection by nifedipine.
12 Testosterone protects against glucotoxicity-induced apoptosis of pancreatic beta-cells (INS-1) and male mouse pancreatic islets.
13 Autosomal dominant diabetes arising from a wolfram syndrome 1 mutation.