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ActinSensor SIGNED

Identification and characterization of a novel damage sensor for cytoskeletal proteins in Drosophila

Total Cost €

0

EC-Contrib. €

0

Partnership

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 ActinSensor project word cloud

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

patterns    cells    screens    serves    diversity    molecules    molecular    extracellular    drosophila    return    endogenous    candidate    cell    myocardial    serve    stroke    organisms    mammals    tissue    elicits    function    functionally    homolog    damaged    innate    secondary    signals    implicated    silico    jak    fruit    immunobiology    infection    damps    inflammatory    presentation    stimuli    lectin    list    contributor    cross    homeostasis    candidates    mediated    dngr    signalling    stat    sensing    evolution    vivo    recruit    gain    obscure    dngr1    expressed    actin    insights    laboratory    atp    biochemical    fly    give    sensor    immune    vertebrates    release    damp    dependent    evolutionary    thought    dcs    noxious    discovered    transduction    injury    conduct    modulate    cd8    recognised    sterile    transplantation    mediating    anticipate    damage    sensors    rnai    vitro    death    uric    dendritic    genetic    sudden    receptor    elicit    cytoskeletal    validate    host    conserved    screen    inflammation    tissues    dead    independently    infarction    counteract    functional    melanogaster    acid    antigen    multiple   

Project "ActinSensor" data sheet

The following table provides information about the project.

Coordinator
THE FRANCIS CRICK INSTITUTE LIMITED 

Organization address
address: 1 MIDLAND ROAD
city: LONDON
postcode: NW1 1AT
website: www.crick.ac.uk

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 United Kingdom [UK]
 Total cost 195˙454 €
 EC max contribution 195˙454 € (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 2019
 Duration (year-month-day) from 2019-01-01   to  2020-12-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE FRANCIS CRICK INSTITUTE LIMITED UK (LONDON) coordinator 195˙454.00

Map

 Project objective

Inflammation is a host response that evolved to counteract noxious stimuli that result from infection or tissue injury, and serves to return the affected tissue to homeostasis. Cell death-associated sterile inflammation is a major contributor to secondary tissue damage associated with multiple conditions such as myocardial infarction, transplantation, and stroke. Damaged tissues are thought to elicit their inflammatory effects through the sudden release from cells of endogenous Damage-Associated Molecular patterns (DAMPs) that serve to recruit and modulate the function of immune cells. In vertebrates, a diversity of molecules have been implicated as DAMPs, including ATP, uric acid, and F-actin. In mammals, F-actin is recognised as a DAMP by the C-type lectin receptor DNGR1, expressed on CD8 Dendritic cells (DCs), that signals to favour the cross-presentation of dead-cell antigen to CD8 T-cells. Independently of its work on DNGR-1, the host laboratory discovered that extracellular actin elicits a JAK-STAT-dependent inflammatory response in the fruit fly (Drosophila melanogaster). DNGR-1 does not have a functional homolog in fly, therefore the actin sensor remains obscure. In order to identify the molecular sensor of extracellular actin we have conducted an in silico-based screen to identify a candidate list of potential sensors. To functionally evaluate these candidates, we will conduct in vivo RNAi and in vitro gain-of-function screens in Drosophila. We will validate the role for this novel sensor in mediating sensing of extracellular actin through multiple genetic and biochemical approaches. We expect our proposal to give novel insights into the signalling transduction and immunobiology of host responses to evolutionary conserved DAMPs. We anticipate that by understanding cytoskeletal-mediated innate inflammatory responses in fly, it will provide important insights into the evolution of similar damage sensor response pathways in higher organisms

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