Dieter Rondas

TL;DR: Inflammatory stress, induced by the cytokines interleukin-1β and interferon-γ, leads to citrullination of GRP78 in β-cells, which generates a novel autoantigen in type 1 diabetes, opening new avenues for biomarker development and therapeutic intervention.

TL;DR: The data demonstrate that high concentrations of glucose induce ER and oxidative stress, which causes cell death mediated by Bim and Puma, which indicates that inhibition of BIM and Pum, or their inducers, may prevent beta-cell destruction in type 2 diabetes.

TL;DR: Results indicate that glucose-induced activation of FAK, paxillin, and ERK1/2 is mediated by β1 integrin intracellular signaling, a mechanism whereby FAK mediates glucose- induced actin cytoskeleton remodeling, hence allowing docking and fusion of insulin granules to the plasma membrane, and a possible functional role for the Akt/AS160 signaling pathway in the FAK-mediated regulation of glucose-stimulated insulin secretion.

TL;DR: Glucose-stimulated remodeling of focal adhesions and phosphorylation of FAK and paxillin are involved in full development of GSIS, indicating a previously unknown role for focal adhesion remodeling in pancreatic β-cell function.

TL;DR: It is suggested that inflammatory cytokines induce a self-destructive pro-apoptotic feedback loop through the secretion and membrane translocation of GRP78, opening the road for the use of compounds that block sGRP78 as potential beta cell-preserving therapies in type 1 diabetes.