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FIRM SIGNED

Form and Function of the Mitochondrial Retrograde Response

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 FIRM project word cloud

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

resistance    uncontrolled    form    sustain    defective    cells    hypothesise    substrates    axis    modulate    remodelled    reactive    mitochondria    energy    trafficking    cholesterol    elucidating    treatment    bi    retrograde    expertise    biogenesis    domains    protocols    cytoprotective    proliferative    mechanism    retro    capitalizes    core    counteract    oncogenic    species    steroids    uncharacterized    molecules    describing    demonstrated    anterograde    nuclear    validating    therapeutic    communication    exerted    nucleus    sensors    metabolic    induce    generating    experimental    reprogramming    stands    cellular    cell    mrr    signalling    crosstalk    plan    ca2    autophagy    microdomains    exploited    ros    regulation    mitochondrial    mechanistic    metabolism    communicate    benefit    effectors    escaped    function    cytosolic    molecular    directional    unveil    preventive    expedite    ranging    meet    synthesis    dysregulated    stressed    oxygen    intermediates    rapid    determinant    environment    deficiencies    diagnostic    unveiling    enriched    mito    interrogate    abnormal   

Project "FIRM" data sheet

The following table provides information about the project.

Coordinator
THE ROYAL VETERINARY COLLEGE 

Organization address
address: ROYAL COLLEGE STREET
city: LONDON
postcode: NW1 OTU
website: www.rvc.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 1˙450˙060 €
 EC max contribution 1˙450˙060 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2018-COG
 Funding Scheme ERC-COG
 Starting year 2019
 Duration (year-month-day) from 2019-04-01   to  2024-03-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE ROYAL VETERINARY COLLEGE UK (LONDON) coordinator 1˙450˙060.00

Map

 Project objective

The molecular communication between mitochondria and nucleus is an integrated bi-directional crosstalk - anterograde (nucleus to mitochondria) and retrograde (mitochondria to nucleus) signalling pathways. The mitochondrial retrograde response (MRR) is driven by defective mitochondrial function, which increases cytosolic reactive oxygen species (ROS) and Ca2. Metabolic reprogramming is a key feature in highly proliferative cells to meet the energy needs for rapid growth by generating substrates for cellular biogenesis. In these mitochondria retro-communicate with the nucleus to induce wide-ranging cytoprotective effects exploited to develop resistance against treatment and sustain uncontrolled growth. Recently, the mitochondrial management of cholesterol-derived intermediates for the synthesis of steroids has been demonstrated as a determinant in the oncogenic reprogramming of cellular environment. We hypothesise that cholesterol-enriched domains facilitate the communication between remodelled mitochondria and nucleus to expedite MRR. This mechanism may be exploited during abnormal cell growth in which cholesterol metabolism and associated molecules are increased. This application capitalizes on expertise in cell signalling and metabolism to interrogate core pathways and unveil molecular sensors and effectors that define form and function of the MRR by: I. Elucidating the mechanism of metabolic regulation of MRR, describing the role exerted by cholesterol trafficking; II. Unveiling microdomains for mito-nuclear communication established by remodelled, autophagy escaped, mitochondria; III. Validating protocols to modulate and target MRR for diagnostic and therapeutic benefit; The experimental plan will (i) define a molecular signalling axis that currently stands uncharacterized, (ii) provide mechanistic knowledge for preventive, and (iii) therapeutic applications to counteract deficiencies associated with stressed, dysregulated mitochondria.

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