NOD2 SIGNALLING

Elucidating the molecular mechanism of NOD2-mediated autophagy

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

 Organization address address: University Offices, Wellington Square
city: OXFORD
postcode: OX1 2JD

contact info
Titolo: Dr.
Nome: Stephen
Cognome: Conway
Email: send email
Telefono: +44 1865 289800
Fax: +44 1865 289801

 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 199˙549 €
 EC contributo 199˙549 €
 Programma FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call FP7-PEOPLE-2010-IEF
 Funding Scheme MC-IEF
 Anno di inizio 2011
 Periodo (anno-mese-giorno) 2011-04-01   -   2013-03-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD

 Organization address address: University Offices, Wellington Square
city: OXFORD
postcode: OX1 2JD

contact info
Titolo: Dr.
Nome: Stephen
Cognome: Conway
Email: send email
Telefono: +44 1865 289800
Fax: +44 1865 289801

UK (OXFORD) coordinator 199˙549.60

Mappa


 Word cloud

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

dcs    autophagy    bacterial    nod    dendritic    handling    presentation    mdp    stimulation    pathway    antigen    mediated    cells    cd    induces    receptor   

 Obiettivo del progetto (Objective)

'NOD2 is an intracellular pathogen recognition receptor (PRR) expressed in monocyte lineage and intestinal epithelial cells. NOD2 recognizes muramyldipeptide (MDP), a component of bacterial cell walls and MDP stimulation induces a signalling cascade that synergises with that of other PRRs to mature dendritic cells (DCs) and renders them competent for antigen presentation. NOD2 is notable in that variants of the receptor are associated with 40% of western Crohn’s (CD) disease. Previously Dr Simmons group has shown that NOD2 induces autophagy in dendritic cells and that this is required for correct antigen presentation and bacterial handling. CD patient DCs expressing variant NOD2 show defective autophagy induction, impaired bacterial handling and antigen presentation. This combination of effects could predispose to inflammation by allowing abnormal persistence of bacterial components in the mucosa. Here, the aim is to investigate the mechanism of NOD2-mediated autophagy and to examine NOD2 interacting proteins pre- and post- stimulation with MDP. Furthermore, siRNA library screening will be used to identify genes that participate in the NOD2 autophagy pathway. Elucidating the special features of NOD2-mediated autophagy is essential to develop targeted immunomodulators of this pathway.'

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