Opendata, web and dolomites

RepliStressTiming TERMINATED

Impact of replicative stress on DNA replication timing control

Total Cost €

0

EC-Contrib. €

0

Partnership

0

Views

0

 RepliStressTiming project word cloud

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

chromatin    timing    defects    connection    tumorigenesis    prevents    safeguards    instability    hypothesize    silencing    vicinity    signaling    syndrome    select    maintains    components    inform    laying    characterization    oncogene    corresponding    regulated    gene    transcriptomics    idea    alludes    atr    driver    functional    master    pathologies    indicating    cancer    suppressors    caused    mechanisms    replication    mechanistic    seckel    primary    models    hereditary    regulating    emerged    skills    perturbations    patterns    tumor    striking    deficient    prominent    activation    basis    independent    dna    status    potentially    direct    first    cellular    foundations    bridging    diseases    replicated    perturbs    stalled    mediated    leads    genomic    kinase    substantiated    biology    expression    vivo    determines    underlying    loci    preliminary    career    stress    form    defective    gain    therapeutics    damage    repercussions    regulator    genomics    altered    transcriptional    disruption    outcomes    alters    complement    carefully    poorly    forks    inhibitors    expertise    genes    shifts   

Project "RepliStressTiming" data sheet

The following table provides information about the project.

Coordinator
KOBENHAVNS UNIVERSITET 

Organization address
address: NORREGADE 10
city: KOBENHAVN
postcode: 1165
website: www.ku.dk

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 Denmark [DK]
 Project website http://www.cpr.ku.dk/research/proteinsignaling/mailand/
 Total cost 200˙194 €
 EC max contribution 200˙194 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2016
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2017
 Duration (year-month-day) from 2017-06-01   to  2019-05-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    KOBENHAVNS UNIVERSITET DK (KOBENHAVN) coordinator 200˙194.00

Map

 Project objective

Replication stress has emerged as a prominent driver of genomic instability. The ATR kinase is a master regulator of the cellular response to replication stress and defects in ATR activation or loss of its signaling components leads to DNA damage, genomic instability and tumorigenesis. Yet the direct mechanisms by which ATR signaling prevents these repercussions remain poorly understood. The primary aim of this study is to investigate a novel role for ATR in regulating the cellular replication timing program and corresponding gene expression. I hypothesize that replication stress caused by disruption of ATR signaling perturbs the carefully regulated timing by which genes are replicated. This directly alters gene expression patterns, potentially leading to oncogene activation and/or silencing of tumor suppressors. This idea is substantiated by my preliminary results indicating striking shifts in replication timing of select genomic loci under defective ATR signaling. Furthermore, a recent finding that ATR maintains the transcriptional status of genes in the vicinity of stalled forks alludes to a similar connection. This timely study will be the first to identify genes with altered transcriptional activity as a result of perturbations in replication timing under ATR-mediated replication stress. Functional characterization of these gene products will provide new insight into how ATR determines replication timing and direct mechanistic basis for how ATR signaling safeguards against tumorigenesis. The outcomes can better inform exploitation of replication stress in cancer therapeutics in the form of ATR inhibitors and underlying pathologies in ATR-deficient Seckel syndrome and associated hereditary diseases. By bridging the fields of replication stress and timing, I will gain new skills in transcriptomics, chromatin biology and in vivo tumor models to complement my previous expertise in replication timing and genomics, laying strong foundations for my independent career.

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

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

CoCoNat (2019)

Coordination in constrained and natural distributed systems

Read More  

PaSION (2018)

A longitudinal assessment of treatment experience, symptoms and potential associations with biomarkers in cancer patients undergoing immune checkpoint inhibitor therapy

Read More  

INFORM (2020)

Innovative Electrochemical Multiplex Biosensor for Detection and Quantification of Clinically Relevant Circulating miRNAs

Read More