MITOUPR

Mitochondrial unfolded protein response and the role in ageing

 Coordinatore KLINIKUM DER UNIVERSITAET ZU KOELN 

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 Nazionalità Coordinatore Germany [DE]
 Totale costo 1˙500˙000 €
 EC contributo 1˙500˙000 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2012-StG_20111109
 Funding Scheme ERC-SG
 Anno di inizio 2013
 Periodo (anno-mese-giorno) 2013-01-01   -   2017-12-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    KLINIKUM DER UNIVERSITAET ZU KOELN

 Organization address address: Kerpener Strasse 62
city: KOELN
postcode: 50937

contact info
Titolo: Dr.
Nome: Aleksandra
Cognome: Trifunovic
Email: send email
Telefono: +49 221 4707813

DE (KOELN) hostInstitution 1˙500˙000.00
2    KLINIKUM DER UNIVERSITAET ZU KOELN

 Organization address address: Kerpener Strasse 62
city: KOELN
postcode: 50937

contact info
Titolo: Mrs.
Nome: Renate
Cognome: Peter
Email: send email
Telefono: +49 221 478 6519
Fax: +49 221 478 87752

DE (KOELN) hostInstitution 1˙500˙000.00

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 Word cloud

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protein    signalling    stress    homeostasis    ageing    mammalian    mitochondrial    organelles    environment    aim    pathways    mechanisms    elegans    unfolded    expression    uprmt    mitochondria    pathway    cells    upr    folding   

 Obiettivo del progetto (Objective)

'Cells use sensor pathways compartmentalized in subcellular organelles to recognize stress conditions, including aberrant protein folding, and in response activate gene expression programs aimed at maintaining cell survival and restoring homeostasis. Fine-tuning of the protein-folding environment in organelles like mitochondria is important for adaptive homeostasis and may participate in development of human diseases and ageing. Work in cultured mammalian cells and more recently in Caenorhabditis elegans has highlighted the importance of mechanisms linking perturbations in the protein-folding environment in the mitochondrial matrix to the expression of nuclear genes encoding mitochondrial proteins. This mitochondrial stress pathway is named mitochondrial unfolded protein response. Much of our knowledge regarding the organelle unfolded protein response (UPR) signalling comes from studies of the endoplasmatic reticulum stress response machinery. In contrast, a potential role of mitochondria in UPR pathway is far less defined, and physiologic regulators of this pathway have not been defined. Here I propose three complementary strategies to identify molecular mechanisms and signalling pathways of the mitochondrial unfolded protein response (UPRmt) under different stress conditions and during ageing. My laboratory has experience in using transgenic mice and C. elegans as experimental tools and both of these powerful model systems will be used in this project.

Specific aims of this proposal are: Aim 1. To identify specific substrates of UPRmt Aim 2. To define mechanisms regulating mammalian UPRmt Aim 3. To elucidate the role of UPRmt signalling in ageing'

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