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Signalling-in-NODs

Investigation of the role and mechanism of action of NOD2-mediated isoform selective PI3K signalling in gut immunity and inflammation

Total Cost €

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EC-Contrib. €

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Partnership

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 Signalling-in-NODs project word cloud

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isoform    intrinsic    kinases    unravel    mechanism    protective    anti    components    unmet    evolutionarily    family    strategies    receptor    ibd    conserved    messengers    host    autophagy    innate    either    driving    pathology    susceptibility    microbiology    protection    molecules    discovered    immune    despite    risk    integrate    elucidate    action    gut    animal    signaling    dendritic    domain    p110    underlying    discover    peptides    generate    oligomerization    bowel    nod2    biology    immunity    deleterious    intestinal    molecular    cell    tolerance    regulating    mediated    pi3k    mice    immunology    nlr    proteins    vivo    plan    single    phenomenon    variants    inflammation    genetic    programs    convey    prr    pathogen    gene    delta    inflammatory    orchestrating    functions    chronic    caused    mechanisms    biological    disease    alongside    regulate    therapeutic    societies    pi3ks    little    made    lipid    nucleotide    pharmacological    phenomena    nod    roles    western    linked    models    microbial    initiated    isoforms    phosphoinositide    dysregulated    mutations    recognition   

Project "Signalling-in-NODs" data sheet

The following table provides information about the project.

Coordinator
QUEEN MARY UNIVERSITY OF LONDON 

Organization address
address: 327 MILE END ROAD
city: LONDON
postcode: E1 4NS
website: http://www.qmul.ac.uk

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country United Kingdom [UK]
 Total cost 195˙454 €
 EC max contribution 195˙454 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2016
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2017
 Duration (year-month-day) from 2017-05-01   to  2019-04-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    QUEEN MARY UNIVERSITY OF LONDON UK (LONDON) coordinator 195˙454.00

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 Project objective

Inflammatory bowel disease (IBD) is a complex chronic pathology in western societies. There is an unmet need for new therapeutic strategies which can only be achieved through a better understanding of the molecular mechanisms of host immunity. It is established that dysregulated host innate immune recognition either caused by genetic risk variants in pathogen recognition receptor (PRR) molecules or microbial factors is commonly associated with IBD. A unique PRR family member, Nucleotide oligomerization domain (NOD)2 programs gut immunity and protection through autophagy process initiated by the recognition of microbial peptides. Deleterious mutations in NOD2 and autophagy-associated proteins are linked to IBD susceptibility. Despite the advances made in understanding of the mechanisms underlying NOD2 biology, particularly that of autophagy, very little is known about the cell signaling components and their mechanism regulating autophagy under NOD2 pathway. Recently, I discovered that a single Phosphoinositide 3-kinases (PI3K) isoform p110δ is integrated in NOD2 mediated autophagy process. PI3Ks are an evolutionarily conserved family of signaling molecules that integrate PRR signaling. PI3Ks generate lipid second messengers and regulate mediated immune responses. I now propose to unravel key biological phenomenon by which p110δ PI3K convey host protective functions through NOD2-mediated autophagy, ensuring the gut immunity and tolerance. The aims are to (1) Determine the dendritic cell-intrinsic role and mechanism(s) of action of PI3K isoforms in orchestrating anti-inflammatory processes under NOD2-mediated autophagy. (2) Discover the roles of PI3K isoforms in NLR-mediated intestinal immunity using isoform specific PI3K gene-targeted mice alongside with pharmacological targeting strategies in vivo. My plan is integrated with animal models, immunology, cell biology, microbiology and in vivo inflammation studies to elucidate key biological phenomena driving IBD.

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