PROCARE

Impact of Proteasome Subpopulations on Cardiac Remodeling

 Coordinatore UNIVERSITAETSKLINIKUM HEIDELBERG 

 Organization address address: IM NEUENHEIMER FELD 672
city: HEIDELBERG
postcode: 69120

contact info
Titolo: Mr.
Nome: Thomas
Cognome: Eisenhauer
Email: send email
Telefono: +49 6221 567324
Fax: +49 6221 565460

 Nazionalità Coordinatore Germany [DE]
 Totale costo 100˙000 €
 EC contributo 100˙000 €
 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-CIG
 Funding Scheme MC-CIG
 Anno di inizio 2012
 Periodo (anno-mese-giorno) 2012-01-01   -   2015-12-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITAETSKLINIKUM HEIDELBERG

 Organization address address: IM NEUENHEIMER FELD 672
city: HEIDELBERG
postcode: 69120

contact info
Titolo: Mr.
Nome: Thomas
Cognome: Eisenhauer
Email: send email
Telefono: +49 6221 567324
Fax: +49 6221 565460

DE (HEIDELBERG) coordinator 100˙000.00

Mappa


 Word cloud

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complexes    proteasomal    cardiac    proteasome       heart    remodeling    ups    disease    hypertrophy   

 Obiettivo del progetto (Objective)

'Heart disease is the number one cause of death in Europe and the world. Cardiac remodeling involving cardiac hypertrophy is associated with higher morbidity as well as mortality due to heart disease. Cardiac muscle mass is potentially influenced by the ubiquitin proteasome system (UPS). At the heart of the UPS is the proteasome, which specifically degrades targeted proteins into peptides. The candidate has identified that the cardiac proteasomal core, the 20S proteasome, is a heterogenic group of highly similar multiprotein complexes with different functionality. During the development of cardiac hypertrophy, the assembly and thus the composition of 20S proteasome complexes is distinctly regulated. In consequence, proteasomal activities change non-uniformly. The objective of the proposed study is to analyze the impact of this regulatory mechanism on cardiac remodeling.'

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