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ATR-mediated mechanotransduction and connections with the actin cytoskeleton

Total Cost €


EC-Contrib. €






 MECHANOCHECK project word cloud

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

explore    laboratory    occurs    primarily    oncogenic    found    cancer    associates    anti    techniques    linking    actin    topological    nucleus    mechanotransduction    barrier    suggest    atr    act    breakdown    mechanism    microscopy    afm    dna    defective    multidisciplinary    aberrant    genes    relevance    force    chromatin    accompanied    association    transitions    exhibit    osmotic    molecular    mechanical    systematically    prophase    hypothesis    microfluidic    device    prevents    micropatterned    stimuli    chromosomes    employ    mutated    plasticity    connections    observations    integrity    cells    modulation    ddr    cytoskeleton    cell    atomic    cellular    forms    chk2    biology    envelope    prompted    fragile    extracellular    nuclear    protein    substrate    functional    microenvironment    unclear    stress    protects    mechanosensing    replicating    mediated    atm    expression    questions    quantitatively    events    kinase    condensation    damage    chk1    controls    foiani    cope    site   

Project "MECHANOCHECK" data sheet

The following table provides information about the project.


Organization address
address: VIA ADAMELLO 16
city: MILANO
postcode: 20139

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 180˙277 €
 EC max contribution 180˙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


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 


 Project objective

The ATR protein kinase controls the DNA damage response (DDR), with ATM, Chk1 and Chk2. DDR genes are often mutated in cancer cells and act as an anti-cancer barrier in response to oncogenic stimuli. ATR is essential and protects the integrity of replicating chromosomes, prevents fragile site expression and aberrant condensation events. The Foiani laboratory recently found that ATR associates with the nuclear envelope during S phase and prophase and in response to osmotic or mechanical stress. Moreover, ATR-defective cells exhibit aberrant chromatin condensation and nuclear envelope breakdown. These observations prompted us to suggest that the ATR-mediated mechanical response enables cells to cope with the mechanical stress induced by topological transitions through the modulation of nuclear plasticity and chromatin association to the nuclear envelope. However, the molecular mechanism and functional relevance of ATR-mediated mechanical response remain unclear. Mechanosensing occurs primarily through the actin cytoskeleton, which forms the cellular mechanical system linking the extracellular microenvironment to the nucleus. We aim at understanding the connections between the ATR-mediated mechanotransduction pathway and actin modulation in response to mechanical stress. Our working hypothesis is that ATR may be part of an integrated response to mechanical stress that has a more general role in controlling cell and nuclear plasticity through the modulation of actin cytoskeleton and nuclear events. To address these questions, we will employ and develop various multidisciplinary approaches including state-of-the-art Atomic Force Microscopy (AFM), micropatterned protein substrate, novel microfluidic device and accompanied with advanced molecular biology techniques in order to quantitatively and systematically explore the ATR mediated mechanotransduction.

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

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