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FIRM SIGNED

Form and Function of the Mitochondrial Retrograde Response

Total Cost €

0

EC-Contrib. €

0

Partnership

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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.

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

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

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

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