XBP1 and Endoplasmic Reticulum Stress in Mucosal Homeostasis
Endoplasmic reticulum (ER) stress allows cells to cope with misfolded proteins through the Unfolded Protein Response (UPR). We have recently reported that unabated ER stress, a consequence of genetic deletion of X-box binding prot...
ver más
¿Tienes un proyecto y buscas un partner? Gracias a nuestro motor inteligente podemos recomendarte los mejores socios y ponerte en contacto con ellos. Te lo explicamos en este video
Fecha límite de participación
Sin fecha límite de participación.
Descripción del proyecto
Endoplasmic reticulum (ER) stress allows cells to cope with misfolded proteins through the Unfolded Protein Response (UPR). We have recently reported that unabated ER stress, a consequence of genetic deletion of X-box binding protein-1 (XBP1), in intestinal epithelial cells (IECs) leads to intestinal inflammation reminiscent of inflammatory bowel disease (IBD), and polymorphisms in XBP1 were associated with Crohn s disease and ulcerative colitis.
The current proposal is based on this central discovery, and rests on three major pillars. 1. Elucidation of the molecular pathways that connect unabated ER stress with inflammation, with the potential to identify novel therapeutics. 2. Testing the hypothesis that XBP1 deficiency may regulate colorectal cancer development, both sporadic and inflammation-associated. 3. Addressing the hypothesis that XBP1 and ER stress may contribute to the molecular pathology of primary sclerosing cholangitis (PSC) via affecting cholangiocyte biology. Insight from these studies may have implications well beyond mucosal inflammation as ER stress mechanisms have been suggested to play a role in a wide variety of diseases.