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IntestineUb

The role of Ubiquitin System on the homeostatic control of stem cell maintenance and differentiation in crypt stem cells

Total Cost €

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EC-Contrib. €

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Partnership

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 IntestineUb project word cloud

Explore the words cloud of the IntestineUb project. It provides you a very rough idea of what is the project "IntestineUb" about.

localization    mammalian    cellular    tissue    pattern    renewal    sustain    stem    amenable    phenotype    maintenance    sized    conditional    caused    gene    differentiation    homeostatic    fuelled    organoid    technologies    transcriptional    arrayed    performing    sub    vivo    essentially    ubiquitin    regulation    powerful    proteins    function    ubiquitination    signalling    crypt    knockout    reporter    expression    either    mutation    proteome    cas9    screening    vitro    advantage    regarding    intestine    self    optimal    recapitulates    mis    components    mass    homeostasis    cells    cell    attenuate    organization    mechanism    modifications    candidate    hyperplasia    adult    primary    extensively    rate    culture    tight    ligases    biochemical    adequately    epithelium    mouse    small    biological    modification    tissues    near    model    multipotency    post    reside    characterization    organoids    serves    intestinal    conducting    population    bioid    assay    experimental    little    effect    surface    ip    elucidate    molecule    models    translational    crispr    generation    inhibitors    lines    e3   

Project "IntestineUb" data sheet

The following table provides information about the project.

Coordinator
THE CHANCELLOR MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE 

Organization address
address: TRINITY LANE THE OLD SCHOOLS
city: CAMBRIDGE
postcode: CB2 1TN
website: www.cam.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]
 Project website https://www.imba.oeaw.ac.at/research/bon-kyoung-koo/
 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-2014
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2016
 Duration (year-month-day) from 2016-01-01   to  2018-11-01

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE CHANCELLOR MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE UK (CAMBRIDGE) coordinator 195˙454.00

Map

 Project objective

The epithelium of small intestine has a higher self-renewal rate than any other mammalian tissues. This is fuelled by the intestinal stem cells which reside near the bottom of crypt. Tight regulation of the adult stem cell number is required to sustain an adequately sized population for optimal tissue homeostasis. Mis-regulation of homeostasis results in either hyperplasia or loss of stem cells. Although transcriptional regulation of stem cell homeostasis regarding multipotency and differentiation has been extensively studied, only little is known about post-translational modifications. A key mechanism of post-translational modification is ubiquitination by the ubiquitin system (US).

The in vitro primary intestinal organoid culture system recapitulates in vivo epithelium organization, is amenable to essentially all experimental technologies that have been developed for cell lines, and therefore serves as a novel, robust and powerful model system. Taking advantage of the intestinal organoids, this project is aimed to investigate the role of US on the homeostatic control of stem cell maintenance and differentiation in crypt stem cells by: 1. Screening of US required for stem cell number regulation by CRISPR/Cas9 technology; 2. Characterization of the expression pattern and sub-cellular localization of candidate US; 3. Examining the effect of candidate US in signalling pathways involved in the homeostatic control by reporter assay and target gene expression; 4. Identifying target proteins of candidate US using surface proteome analysis, IP-mass, BioID or in vitro ubiquitination of arrayed proteins; 5. Performing biochemical and cell biological analysis of candidate US with its identified target proteins and signalling pathway components in vitro; 6. Generation of conditional knockout mouse models to elucidate the function of candidate US in vivo; 7. Conducting a small molecule screening for inhibitors that attenuate hyperplasia phenotype caused by E3 ligases mutation.

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The information about "INTESTINEUB" are provided by the European Opendata Portal: CORDIS opendata.

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