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ENVERESP SIGNED

Crosstalk between nuclear envelope and DNA Damage Response: Role of nucleoporin TPR in the maintenance of genomic integrity

Total Cost €

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EC-Contrib. €

0

Partnership

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 ENVERESP project word cloud

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

tpr    mutagenesis    atm    previously    solid    ddr    extensive    domain    silac    survival    pediatric    region    replication    genome    barrier    signal    intracranial    ing    imaging    proto    electron    fused    serves    oncogenesis    kinases    leads    proteomic    employing    genes    treatments    raf    promoter    ependymomas9    liver    human    dna    types    kinase    receives    their    responsive    protein    breast    development2    domains    cancer8    linked    chromatin    mutation    genomics    cancer    microscopy    lesions    molecular    body    genesis    nuclear    vitro    prevents    mechanistic    envelope    found    phosphorylated    optimize    stability    checkpoint    biological    critical    each    threats    deregulated    interestingly    amplification    terminal    translocated    network    profiling    met    significantly    pore    tumors    damage    cell    condensation    counteract    expression    technologies    patients    posed    networks    repair    shorter    damaged    therapies    detect    tumor    oncogenes    progression    principles    atr    nucleoporin    signaling    maintenance    binding    thousands    genetics    proteins    day    proteomics    mechanism    cells   

Project "ENVERESP" data sheet

The following table provides information about the project.

Coordinator
IFOM FONDAZIONE ISTITUTO FIRC DI ONCOLOGIA MOLECOLARE 

Organization address
address: VIA ADAMELLO 16
city: MILANO
postcode: 20139
website: www.ifom-firc.it

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 Italy [IT]
 Total cost 168˙277 €
 EC max contribution 168˙277 € (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 2016-04-01   to  2018-03-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    IFOM FONDAZIONE ISTITUTO FIRC DI ONCOLOGIA MOLECOLARE IT (MILANO) coordinator 168˙277.00

Map

 Project objective

Each cell in the human body receives thousands of DNA lesions per day. To counteract threats posed by DNA damage, cells have evolved an integrated signaling network called the DNA-damage response (DDR). This mechanism allows cells to detect DNA lesions, signal their presence and promote their repair. Mutation of DDR genes, which serves as a biological barrier against tumor progression, leads to cancer development2. A large-scale proteomic analysis of proteins phosphorylated in response to DNA damage by checkpoint kinases ATM and ATR identified extensive protein networks responsive to DNA damage. Interestingly, among the proteins identified to be phosphorylated upon DNA damage were several nuclear pore complex factors including nucleoporin Translocated Promoter Region (TPR)5. TPR was previously linked to cancer since its N-terminal domain has been found fused with the protein kinase domains of various proto-oncogenes such as RAF and MET resulting in human solid tumors. TPR expression level was found deregulated in many types of human tumors such as breast and liver cancer8. Amplification of TPR was also significantly associated with a shorter survival of patients with pediatric intracranial ependymomas9. All these findings support a critical role for TPR in the mechanism of oncogenesis. By employing state-of-the-art proteomics (SILAC), genetics (in vitro mutagenesis), genomics (DNA binding profiling) and imaging (electron microscopy) technologies we will investigate how TPR prevents tumor genesis via its role in the DDR network coordinating DNA repair, DNA replication and chromatin condensation with the nuclear envelope upon DNA damage. Providing mechanistic insight into the role of TPR in DDR and the maintenance of genome stability will not only contribute to our understanding of molecular principles of response to damaged DNA, but will allow us to optimize existing cancer treatments and design new molecular targeted therapies in the future.

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