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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.

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

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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