MUCOSAL ER STRESS

XBP1 and Endoplasmic Reticulum Stress in Mucosal Homeostasis

Coordinatore	THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
Nazionalità Coordinatore	United Kingdom [UK]
Totale costo	1˙500˙000 €
EC contributo	1˙500˙000 €
Programma	FP7-IDEAS-ERC Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	ERC-2010-StG_20091118
Funding Scheme	ERC-SG
Anno di inizio	2011
Periodo (anno-mese-giorno)	2011-01-01   -   2015-12-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE  Organization address address: The Old Schools, Trinity Lane city: CAMBRIDGE postcode: CB2 1TN contact info Titolo: Dr. Nome: Arthur Cognome: Kaser Email: send email Telefono: +44 1223 336808 Fax: +44 1223 336846	UK (CAMBRIDGE)	hostInstitution	1˙500˙000.00
2	THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE  Organization address address: The Old Schools, Trinity Lane city: CAMBRIDGE postcode: CB2 1TN contact info Titolo: Ms. Nome: Renata Cognome: Schaeffer Email: send email Telefono: 44122333543 Fax: 441223000000	UK (CAMBRIDGE)	hostInstitution	1˙500˙000.00

Mappa

 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

 Obiettivo del progetto (Objective)

'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.'