thapsigargin and Celiac-Disease

Celiac disease (CD) is an inflammatory intestinal disease caused by the ingestion of gluten-containing cereals by genetically predisposed individuals. Constitutive differences between cells from CD patients and control subjects, including levels of protein phosphorylation, alterations of vesicular trafficking, and regulation of type 2 transglutaminase (TG2), have been reported. In the present work, we investigated how skin-derived fibroblasts from CD and control subjects responded to thapsigargin, an endoplasmic reticulum ER stress inducer, in an attempt to contribute to the comprehension of molecular features of the CD cellular phenotype. We analyzed Ca

Topics: Autophagy; Celiac Disease; GTP-Binding Proteins; Homeostasis; Humans; Protein Glutamine gamma Glutamyltransferase 2; Thapsigargin; Transglutaminases