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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.

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

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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