ADAM-15 AND AF

Evaluation of ADAM-15 in atrial fibrillation

 Coordinatore LUDWIG-MAXIMILIANS-UNIVERSITAET MUENCHEN 

 Organization address address: GESCHWISTER SCHOLL PLATZ 1
city: MUENCHEN
postcode: 80539

contact info
Titolo: Prof.
Nome: Stefan
Cognome: Kääb
Email: send email
Telefono: 498971000000
Fax: 498971000000

 Nazionalità Coordinatore Germany [DE]
 Totale costo 252˙742 €
 EC contributo 252˙742 €
 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-2012-IOF
 Funding Scheme MC-IOF
 Anno di inizio 2013
 Periodo (anno-mese-giorno) 2013-06-01   -   2016-05-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    LUDWIG-MAXIMILIANS-UNIVERSITAET MUENCHEN

 Organization address address: GESCHWISTER SCHOLL PLATZ 1
city: MUENCHEN
postcode: 80539

contact info
Titolo: Prof.
Nome: Stefan
Cognome: Kääb
Email: send email
Telefono: 498971000000
Fax: 498971000000

DE (MUENCHEN) coordinator 252˙742.20

Mappa


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he    clauss    electrophysiology    training    dr    mouse    genetic    variants    career    af    risk    skills    candidate    adam   

 Obiettivo del progetto (Objective)

'Atrial fibrillation (AF) is the most common arrhythmia in Europe affecting more than 6 million people. AF is associated with significant mortality and morbidity including an increased risk for stroke, dementia and heart failure. Thus, AF is a major healthcare burden. The pathophysiology of AF is complex and still not fully understood. Increasing data support a genetic component to AF. Genome-wide association studies (GWAS) identified genetic variants associated with increased susceptibility for AF. However, the mechanism by which genetic variants influence the risk for AF is still unknown. At one AF risk locus with many genes, the top SNP is related to transcriptional levels of the metalloproteinase ADAM-15. Since ADAM-15 can activate inflammatory cytokines and regulate extracellular matrix turnover, it is a strong candidate gene for AF. To investigate the role of ADAM-15 in AF, the candidate, Dr. Sebastian Clauss, will characterize the cardiac phenotype of an ADAM-15 knockout mouse model. Dr. Clauss proposes to seek postdoctoral training in the laboratory of Dr. Patrick Ellinor at Massachusetts General Hospital and Harvard Medical School. During his training he will acquire new skills for characterizing mice including electrocardiography, echocardiography, invasive hemodynamics, electrophysiology (EP) studies, and optical mapping. This training opportunity would be a crucial step in Dr. Clauss’ career development as it will not only expand his scientific skills it will also enable the transfer of his knowledge and experience to Europe upon his return. Finally, he will establish a mouse electrophysiology facility in Munich that will provide the basis for his future career as an independent researcher and will further increase European research excellence.'

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