SIRTUINS

Phenogenomics of sirtuin corepressor family

 Coordinatore ECOLE POLYTECHNIQUE FEDERALE DE LAUSANNE 

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 Nazionalità Coordinatore Switzerland [CH]
 Totale costo 2˙485˙000 €
 EC contributo 2˙485˙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-2008-AdG
 Funding Scheme ERC-AG
 Anno di inizio 2009
 Periodo (anno-mese-giorno) 2009-02-01   -   2014-01-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    ECOLE POLYTECHNIQUE FEDERALE DE LAUSANNE

 Organization address address: BATIMENT CE 3316 STATION 1
city: LAUSANNE
postcode: 1015

contact info
Titolo: Ms.
Nome: Caroline
Cognome: Vandevyver
Email: send email
Telefono: +41 21 693 4977
Fax: +41 21 693 5585

CH (LAUSANNE) hostInstitution 2˙485˙000.00
2    ECOLE POLYTECHNIQUE FEDERALE DE LAUSANNE

 Organization address address: BATIMENT CE 3316 STATION 1
city: LAUSANNE
postcode: 1015

contact info
Titolo: Prof.
Nome: Johan
Cognome: Auwerx
Email: send email
Telefono: -1624
Fax: +41-21-693 9600

CH (LAUSANNE) hostInstitution 2˙485˙000.00

Mappa


 Word cloud

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models    natural    sirtuin    gemms    cellular    deacetylation    metabolism    mouse    linked    metabolic    genetic    populations    impact    human    tissue    sirtuins    grps    genetically    gene   

 Obiettivo del progetto (Objective)

'By modulating the activity of transcription factors, cofactors influence cellular and organismal metabolic pathways. Recently the role of the sirtuin cofactor gene family received a lot of attention in this context, as their beneficial impact on longevity was linked to effects on metabolic control. Most sirtuins catalyze deacetylation reactions that are tightly linked to cellular energy (NAD) levels. To ascertain the tissue-specific contributions of sirtuins in metabolism, we propose here to: 1) identify novel deacetylation targets for the sirtuins; 2) generate and characterize genetically engineered mouse models (GEMMs) with somatic mutations in the 7 sirtuin genes in liver, muscle and adipose tissue, key metabolic tissues; 3) study mouse models with natural genetic variation in sirtuin expression, such as found in genetic reference populations (GRPs), like the BxD recombinant inbred mouse lines; and 4) validate the relevance of sirtuin signaling for human metabolism through clinical genetic studies. As the goal is to progress towards the treatment and prevention of metabolic diseases in humans, GEMMs are optimized to study the actions of isolated genetic loci and are thus insufficient to characterize polygenic networks and genetic interactions. Moreover environmental factors can impact on the manifestations of the genotype or phenocopy the genetically produced phenotype. Thus, to dissect complex genetic traits, experimental models, like GRPs, that imitate the genetic structure of human populations provide complimentary information to that obtained from GEMMs. As we will combine data generated using directional genetic strategies in GEMMs with a high-throughput phenogenomic analysis of GRPs, our approach merges the benefits of clear-cut results of single gene perturbations in a given tissue with subtle alterations that result from natural innumerable allelic variants. This will ultimately favor the definition of the role of the sirtuins in metabolic homeostasis.'

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