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mitoUPR SIGNED

Cellular modulation by the mitochondrial unfolded protein response

Total Cost €

0

EC-Contrib. €

0

Partnership

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 mitoUPR project word cloud

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

combined    uprmt    human    severe    paracrine    holds    misfolding    poorly    restore    worms    cytosolic    cutting    therapeutic    proteostasis    metabolism    additionally    translation    mechanisms    organism    balance    mammalian    cell    composition    energy    acutely    signal    organismal    cancer    stress    neighboring    exerts    inducing    mitochondrial    ipsc    cytosol    ought    unknown    influence    signaling    possibility    generation    neurodegenerative    activate    cellular    folding    compartments    sequencing    undescribed    endocrine    protein    modification    direct    uncover    function    carries    model    spectrometry    newly    questions    granules    central    environment    editing    tools    diseases    strikingly    layer    adjustments    autonomous    gene    regulation    notably    environments    edge    modulating    quantitative    rna    induce    homeostasis    implications    microscopy    unfolded    disease    robustness    mitochondria    proliferation    mass    cells    extensive    treatment   

Project "mitoUPR" data sheet

The following table provides information about the project.

Coordinator
JOHANN WOLFGANG GOETHE-UNIVERSITATFRANKFURT AM MAIN 

Organization address
address: THEODOR W ADORNO PLATZ 1
city: FRANKFURT AM MAIN
postcode: 60323
website: www.uni-frankfurt.de

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 Germany [DE]
 Total cost 1˙437˙500 €
 EC max contribution 1˙437˙500 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2018-STG
 Funding Scheme ERC-STG
 Starting year 2019
 Duration (year-month-day) from 2019-02-01   to  2024-01-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    JOHANN WOLFGANG GOETHE-UNIVERSITATFRANKFURT AM MAIN DE (FRANKFURT AM MAIN) coordinator 1˙437˙500.00

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 Project objective

Mitochondrial function is central for cellular metabolism and energy balance. However, many diseases, including cancer and neurodegenerative diseases, affect mitochondrial function and proteostasis. Upon mitochondrial protein misfolding, mitochondria activate the mitochondrial unfolded protein response (UPRmt) to restore proteostasis, a poorly characterized pathway in mammalian cells. Notably, the effects of the UPRmt on its direct environment – mitochondria – and on cytosolic homeostasis remain unknown. Strikingly, non-cell autonomous signaling of metabolism and folding state has been described in recent years, particularly in worms. However, the possible role of UPRmt in such processes is undescribed. Using newly available tools to acutely induce the UPRmt in mammalian cells, combined with cutting-edge quantitative mass spectrometry, microscopy, next generation sequencing, and gene editing approaches, we propose to address these important open questions by studying the influence UPRmt exerts on the environments of i) mitochondria (including to study the composition and regulation of RNA granules), ii) cytosol (adjustments of translation, metabolism, and proliferation) and iii) neighboring cells (modification by non-cell autonomous signaling). Additionally, we aim to develop an iPSC-based UPRmt model. On cellular and organismal level, there ought to be mechanisms to signal changes in metabolism and proteostasis to increase robustness in neighboring environments. Studying these effects will be crucial for a better understanding of human disease and carries severe implications: i) the possibility of therapeutic treatment by modulating neighboring compartments or cells and ii) the possibility that diseases inducing the UPRmt could have unknown paracrine and endocrine effects on the organism. This proposal holds the potential to uncover a novel layer of regulation of cellular stress with an extensive influence on our understanding of the UPRmt and disease.

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