METABOMIT

Metabolic consequences of mitochondrial dysfunction

 Coordinatore HELSINGIN YLIOPISTO 

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 Nazionalità Coordinatore Finland [FI]
 Totale costo 2˙500˙000 €
 EC contributo 2˙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-2010-AdG_20100317
 Funding Scheme ERC-AG
 Anno di inizio 2011
 Periodo (anno-mese-giorno) 2011-06-01   -   2016-05-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    HELSINGIN YLIOPISTO

 Organization address address: YLIOPISTONKATU 4
city: HELSINGIN YLIOPISTO
postcode: 14

contact info
Titolo: Ms.
Nome: Berg
Cognome: Tiina
Email: send email
Telefono: +358 9 191 25043

FI (HELSINGIN YLIOPISTO) hostInstitution 2˙500˙000.00
2    HELSINGIN YLIOPISTO

 Organization address address: YLIOPISTONKATU 4
city: HELSINGIN YLIOPISTO
postcode: 14

contact info
Titolo: Prof.
Nome: Anu Elina
Cognome: Wartiovaara
Email: send email
Telefono: +358 9 47171965
Fax: +358 9 4717 1964

FI (HELSINGIN YLIOPISTO) hostInstitution 2˙500˙000.00

Mappa


 Word cloud

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manifestations    models    obese    mitochondrial    thinness    genetically    obesity    pathways    rc    disorders    gene    neurodegeneration    disease    patients    metabolic    unknown    defects   

 Obiettivo del progetto (Objective)

'This proposal aims to clarify mitochondrial contribution to obesity and thinness, using carefully characterized mitochondrial disease and obese patient materials, and genetically modified disease models. Manifestations of mitochondrial respiratory chain (RC) defects range from infantile multisystem disorders to adult-onset myopathies or neurodegeneration, and even aging-related wasting. Why defects in oxidative ATP production can lead to such variety of manifestations and tissue specificity is unknown. We have previously identified a number of gene defects that lead to RC disorders. In addition to neurological symptoms, these patients often show various metabolic manifestations: specific gene defects associate with short stature and thinness, whereas others with metabolic syndrome or obesity. This implies that specific mitochondrial defects can have opposing effects for fat storage or utilization. The involved pathways may contribute to mitochondrial disease progression, but are unknown. We propose to a) undertake a major clinical study on genetically defined, obese or thin, mitochondrial patients, and examine their metabolic phenotype in finest detail. These data will be compared to those from normal obesity, to search for common mechanisms between mitochondrial and general obesity. b) generate a set of disease models for mitochondrial disorders associated with obesity, and knock-out models for specific signallers for crossing with the disease models. c) identify in detail the involved regulatory pathways, and utilize these for searching chemical compounds that could modulate the response, and have therapeutic potential. The project has potential for major breakthroughs in the fields of mitochondrial disease pathogenesis and treatment, neurodegeneration and obesity.'

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