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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 €

0

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.

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

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

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