MUCOSAL ER STRESS

XBP1 and Endoplasmic Reticulum Stress in Mucosal Homeostasis

 Coordinatore THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE 

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 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.

cells    unabated    hypothesis    molecular    intestinal    inflammation    disease    stress    xbp    protein    er   

 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.'

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