INDEFIC

Identification of New Genetic Determinants of Plasma Fibrinogen Concentration

 Coordinatore KAROLINSKA INSTITUTET 

 Organization address address: Nobels Vag 5
city: STOCKHOLM
postcode: 17177

contact info
Titolo: Ms.
Nome: Caroline
Cognome: Hamilton
Email: send email
Telefono: +46 85177 5959
Fax: +46 8337394

 Nazionalità Coordinatore Sweden [SE]
 Totale costo 181˙669 €
 EC contributo 181˙669 €
 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-2009-IEF
 Funding Scheme MC-IEF
 Anno di inizio 2010
 Periodo (anno-mese-giorno) 2010-07-01   -   2013-02-28

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    KAROLINSKA INSTITUTET

 Organization address address: Nobels Vag 5
city: STOCKHOLM
postcode: 17177

contact info
Titolo: Ms.
Nome: Caroline
Cognome: Hamilton
Email: send email
Telefono: +46 85177 5959
Fax: +46 8337394

SE (STOCKHOLM) coordinator 181˙669.40

Mappa


 Word cloud

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

cardiovascular    biological    cvd    independent    genetic    disease    genes    networks    regulation    regions    identification    plasma    tool    risk    concentration    signals    fibrinogen    mechanisms    candidate    variants    pathways    regulatory   

 Obiettivo del progetto (Objective)

'The proposed project aims at the identification and characterization of novel genes, genetic variants and pathways implicated in the regulation of plasma fibrinogen concentration, which is an independent risk factor for cardiovascular disease (CVD). Several genome-wide linkage and association studies have identified some interesting regions which may contain candidate genes that are not yet identified. Despite this exciting progress in narrowing down genomic regions that may be linked to plasma fibrinogen concentration, very few of these signals have actually been dissected to the final causative gene that is responsible for disease susceptibility, and in most instances, the allelic variants and the biological mechanisms underlying these signals remain unknown. Thus, our first and main objective is to dissect already defined candidate regions to identify attractive novel candidate genes and variants that explain variation in plasma fibrinogen concentration. Specifically, we will exploit the novel “expression QTL” methodology as our main tool to prioritize candidate genes in previously described chromosomal regions associated with plasma fibrinogen concentration. This new strategy allows the identification of transcriptional regulatory loci without any prior knowledge of the regulatory mechanism and is now gaining increasing attention as a powerful tool to understand the molecular networks in which candidate genes operate and how changes in these networks lead to changes in disease traits. Accordingly, we expect that it may reveal important novel information about the mechanisms and biological pathways by which some genetic variants may affect plasma fibrinogen regulation. The identification of genes, genetic variants and pathways that influence plasma fibrinogen concentration should lead to a better understanding of the etiology of CVD. Ultimately, the results of these studies should provide clues for developing new strategies for treatment and prevention of CVD.'

Introduzione (Teaser)

Plasma fibrinogen is believed to be an independent risk factor for atherosclerosis, arterial thrombosis and cardiovascular disease (CVD). The EU-funded INDEFIC project is working to identify genes involved in regulating plasma fibrinogen concentration.

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