Opendata, web and dolomites

DNAcheck SIGNED

Mechanistic analysis of DNA damage signaling and bypass upon replication of damaged DNA template in human cells.

Total Cost €

0

EC-Contrib. €

0

Partnership

0

Views

0

 DNAcheck project word cloud

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

shed    activation    assumed    question    re    left    either    budding    seems    unexplored    found    pcna    site    originated    humans    attack    serious    bypass    gaps    predominant    disease    genome    conserved    stability    replicative    fundamental    arises    constitute    multidisciplinary    ssdna    light    cells    stalled    exogenous    interestingly    dna    prevent    association    sensed    function    sources    fork    gap    encounters    yeast    template    networks    molecular    sense    machinery    damaged    leads    exo1    repair    single    damage    clear    uncoupling    extended    mechanism    movement    lagging    generally    poorly    stranded    forks    complete    lesions    signaling    employ    scenario    hence    templates    human    signal    encoded    endogenous    priming    replication    checkpoint    accumulate    stalling    remaining    downstream    breakage    postreplicative    global    mechanisms    helicase    switching    exonuclease    polymerase    strand    constant    synthesis    triggers    actually    restricted    genetic   

Project "DNAcheck" data sheet

The following table provides information about the project.

Coordinator
UNIVERSIDAD DE SEVILLA 

Organization address
address: CALLE S. FERNANDO 4
city: SEVILLA
postcode: 41004
website: www.us.es

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 Spain [ES]
 Total cost 170˙121 €
 EC max contribution 170˙121 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2017
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2018
 Duration (year-month-day) from 2018-10-01   to  2020-09-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSIDAD DE SEVILLA ES (SEVILLA) coordinator 170˙121.00

Map

 Project objective

The genetic information encoded by DNA is under constant attack from both endogenous and exogenous sources of damage. To ensure genome stability and prevent disease, cells use global signaling networks to sense and repair DNA damage. One particularly serious problem is when the replication machinery encounters lesions remaining in the template DNA. In this scenario, cells employ damage bypass mechanisms to complete genome replication and prevent fork breakage. Importantly, these pathways are not restricted to the site of stalling but can also function behind the fork at single-stranded DNA (ssDNA) gaps originated by the re-priming of DNA synthesis downstream of lesions. While it is very well known that ssDNA is the molecular signal that triggers the checkpoint response, it is less clear how and where ssDNA actually arises. Generally, it is assumed to accumulate at stalled replication forks, either by an uncoupling between replicative helicase and polymerase movement or between leading and lagging strand synthesis. However, in a recent study in budding yeast, I found that ssDNA gaps left behind replication forks, and extended by processing factors such as the exonuclease EXO1, constitute the predominant signal that leads to checkpoint activation in response to damaged DNA templates during S phase. Whether this mechanism of checkpoint activation is conserved from yeast to humans remains unexplored. Hence, using a unique set of multidisciplinary approaches, this project aims to address the fundamental question of how DNA damage is sensed during replication in human cells. Interestingly, not only ssDNA gap processing seems important for checkpoint signaling but also for the template switching mechanism of damage bypass. Therefore, this project will also study the function of EXO1 and its association with PCNA at postreplicative ssDNA gaps in order to shed light on the poorly understood mechanism of template switching.

Are you the coordinator (or a participant) of this project? Plaese send me more information about the "DNACHECK" 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 "DNACHECK" are provided by the European Opendata Portal: CORDIS opendata.

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

RAMBEA (2019)

Realistic Assessment of Historical Masonry Bridges under Extreme Environmental Actions

Read More  

PROSPER (2019)

Politics of Rulemaking, Orchestration of Standards, and Private Economic Regulations

Read More  

IRF4 Degradation (2019)

Using a novel protein degradation approach to uncover IRF4-regulated genes in plasma cells

Read More