Opendata, web and dolomites

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

0

Views

0

 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.

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

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.

Are you the coordinator (or a participant) of this project? Plaese send me more information about the "ENVERESP" project.

For instance: the website url (it has not provided by EU-opendata yet), the logo, a more detailed description of the project (in plain text as a rtf file or a word file), some pictures (as picture files, not embedded into any word file), twitter account, linkedin page, etc.

Send me an  email (fabio@fabiodisconzi.com) and I put them in your project's page as son as possible.

Thanks. And then put a link of this page into your project's website.

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

More projects from the same programme (H2020-EU.1.3.2.)

LEVERAGE mRNA (2019)

Laboratory Evolution of Virus-likE pRotein cAGes for Eukaryotic mRNA delivery

Read More  

Migration Ethics (2019)

Migration Ethics

Read More  

NarrowbandSSL (2019)

Development of Narrow Band Blue and Red Emitting Macromolecules for Solution-Processed Solid State Lighting Devices

Read More