COP1-DRP1

Exploring the role of mitochondrial dynamics in tumor regulation by Cop1

 Coordinatore UNIVERSITE DE GENEVE 

 Organization address address: Rue du General Dufour 24
city: GENEVE
postcode: 1211

contact info
Titolo: Prof.
Nome: Luca
Cognome: Scorrano
Email: send email
Telefono: 41223795212
Fax: 41223795260

 Nazionalità Coordinatore Switzerland [CH]
 Totale costo 256˙364 €
 EC contributo 256˙364 €
 Programma FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call FP7-PEOPLE-2011-IEF
 Funding Scheme MC-IEF
 Anno di inizio 2012
 Periodo (anno-mese-giorno) 2012-04-01   -   2014-03-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITE DE GENEVE

 Organization address address: Rue du General Dufour 24
city: GENEVE
postcode: 1211

contact info
Titolo: Prof.
Nome: Luca
Cognome: Scorrano
Email: send email
Telefono: 41223795212
Fax: 41223795260

CH (GENEVE) coordinator 256˙364.20

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

cop    cell    suppressor    mitochondria    accumulation    damage    tumour    functions    dna    cancer    morphology    fission    protein    mitochondrial    drp    death    regulating   

 Obiettivo del progetto (Objective)

'The Constitutive morphogenetic protein 1 (Cop1) is an E3-ubiquitin ligase regulating stability of a broad group of targets with pleiotropic functions. Cop1 emerged as a tumour suppressor in T-cell lymphomas and in prostate cancer. During tumour formation, mitochondria are key organelles regulating cell death and proliferation. This multiplicity of functions is mirrored by the complex morphology of the organelle, resulting from the equilibrium between fusion and fission, events controlled by a set of mitochondria-shaping proteins. Fission depends on the large GTPase dynamin-related protein 1 (DRP1), essential for embryonic development and involved in the control of apoptosis and cell cycle.We found that loss of Cop1 results in increased cell death, DNA damage, mitochondrial fragmentation, and accumulation of D1, highlighting a potential connection between a tumour suppressor and mitochondrial morphology. We therefore hypothesize that Drp1-mediated regulation of mitochondrial morphology participates in tumour suppression by Cop1. To address this hypothesis, we will verify if (i) Drp1 is epistatic to Cop1 in accumulation of DNA damage and sensitivity to cell death; (ii) Drp1 is required for lymphomagenesis in Cop1h/h mice . Our project is expected to establish the role of mitochondrial morphology in Cop1 regulated tumour development.'

Introduzione (Teaser)

Cancer is a complex, multifactorial process and new factors are constantly emerging. A European study looked at how mitochondria protein determinants may influence tumour formation.

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