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Characterising the spatial organisation and regulation of the Wnt receptor complex in stem cells and cancer

Total Cost €


EC-Contrib. €






 WntTraffic project word cloud

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

mechanisms    understand    earliest    tumour    surface    injury    drug    localisation    vital    cell    proliferation    cellular    effectors    events    signal    regeneration    cascade    downstream    endocytosis    combining    cancer    medicine    sub    protein    compartments    biochemistry    regulation    organoid    stem    treatment    elucidate    editing    trafficking    cells    secreted    microscopy    receptors    family    disease    intermediates    wnt    initiation    activation    reservoirs    tools    critical    maintenance    drive    decisive    interactions    tune    gene    bound    homeostasis    glycoproteins    interfere    tool    strategies    central    examine    attractive    molecular    maurice    immuno    turnover    bind    insights    recruitment    employ    receptor    signalling    poorly    laboratory    regenerative    wnts    imaging    electron    genome    intestinal    cytoplasmic    linked    cultures    mediating    meet    endogenous    detect    underlying    deregulated    resolve    tissue    mutations    complexes    trained   

Project "WntTraffic" data sheet

The following table provides information about the project.


Organization address
postcode: 3584 CX

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 Netherlands [NL]
 Project website
 Total cost 177˙598 €
 EC max contribution 177˙598 € (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 2016-04-01   to  2018-03-31


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 


 Project objective

Wnts are a family of secreted glycoproteins that control maintenance and proliferation of stem cell reservoirs during tissue homeostasis and regeneration after injury. Deregulated Wnt signalling due to mutations in important signalling intermediates is strongly linked to disease. The complex molecular mechanisms mediating Wnt-induced cell responses are therefore of wide interest and the underlying protein interactions provide attractive drug targets, particularly in regenerative medicine and cancer treatment.

The earliest events that occur after Wnts bind their receptors at the cell surface, such as receptor endocytosis and recruitment of cytoplasmic effectors, are decisive for downstream gene activation but the underlying mechanisms by which these events process and tune the Wnt signal remain poorly understood. The key objective of this proposal is to resolve critical molecular events that drive initiation of the Wnt cascade in stem and cancer cells. By using a novel tool developed in the Maurice laboratory to detect endogenous Wnt-bound complexes, The Applicant will focus on the following central objectives:

1. To elucidate Wnt receptor localisation in sub-cellular compartments 2. To examine the regulation of Wnt receptor trafficking and turnover in response to Wnt signalling 3. To investigate how cancer cells exploit Wnt receptor trafficking to drive tumour growth

To meet these objectives, The Applicant will be trained to employ an integrated approach combining biochemistry and genome editing in intestinal organoid cultures with advanced imaging including immuno-electron microscopy to develop a unique set of tools to study Wnt receptor trafficking and turnover at the endogenous level. The expected insights will be vital to understand how pathway activation is controlled and for strategies to interfere with Wnt signalling in disease.

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

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