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CAiPSC

Determining centromere assembly mechanisms and improving mitotic fidelity during somatic cell reprogramming

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 CAiPSC project word cloud

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

translational    cells    psc    proliferate    cycle    cell    host    consequently    multifaceted    molecular    atypical    unknown    truncated    fluorescent    g1    function    stem    mitotic    labelling    karyotype    obtain    centromere    regenerative    chromatin    chromosome    assembly    reprogramming    chromosomal    centromeric    strictly    maintenance    regulating    basic    abnormalities    30    researcher    gap    genomic    largely    dependent    mechanisms    central    human    transition    fidelity    maintaining    combination    functional    marks    inheritance    stability    biology    medicine    combining    drive    unusually    extensive    epigenetic    underlying    strategies    somatic    ipscs    pluripotent    pscs    mitosis    direct    ipsc    loci    structure    remodelling    question    rates    techniques    modulation    karyotypic    instability    tightly    segregation    coupled    lines    proper    expertise    genome    capitalises    centromeres    phases    lab    rapid    stable    microscopy    propagation   

Project "CAiPSC" data sheet

The following table provides information about the project.

Coordinator
FUNDACAO CALOUSTE GULBENKIAN 

Organization address
address: AVENIDA BERNA 45
city: LISBOA
postcode: 1000
website: www.igc.gulbenkian.pt

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 Portugal [PT]
 Project website http://www.jansenlab.org/
 Total cost 148˙635 €
 EC max contribution 148˙635 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2015
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2016
 Duration (year-month-day) from 2016-09-01   to  2019-01-28

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    FUNDACAO CALOUSTE GULBENKIAN PT (LISBOA) coordinator 148˙635.00

Map

 Project objective

Maintaining a stable karyotype is essential for the use of pluripotent stem cells (PSCs) in regenerative medicine and translational and basic research. Although around 10-30% of PSC lines present karyotypic abnormalities, the molecular mechanisms underlying this genomic instability are largely unknown. Centromeres, the chromosomal loci that drive chromosome segregation are central to mitotic fidelity. Maintenance of centromeres in somatic cells is tightly cell cycle coupled, as centromeric chromatin assembly is strictly dependent on G1 phase transition. PSCs have an atypical cell cycle structure with truncated gap phases and proliferate at unusually rapid rates. How this affects mitotic fidelity in general, centromere assembly in particular and consequently, genomic stability is an essential question in reprogramming biology. The aim of this multifaceted project is to determine the mechanisms regulating proper chromosome segregation during somatic cell reprogramming to induced PSCs (iPSCs). By combining fluorescent labelling techniques, high-end microscopy and genome-wide analysis, this project will determine the mechanisms of centromere assembly and inheritance in PSCs, the consequences of genome-wide remodelling of chromatin marks during reprogramming on the stable epigenetic propagation of centromeric chromatin and how functional modulation of key centromere assembly factors affect mitotic fidelity. This project capitalises on the unique combination of the researcher’s experience in stem cell biology and iPSC technology and the extensive expertise in the biology of human mitosis and centromere function of the host lab. The results of this study will provide direct insight into how chromosomal segregation is controlled in PSCs and most importantly during reprogramming, which will advance our understanding of the mechanisms underlying the genomic instability of these cells and contribute to the development of strategies to obtain better and more robust iPSCs.

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