CARDIOCLUSTER

The role of ryanodine cluster morphology in arrhythmogenic calcium release after myocardial infarction

 Coordinatore UNIVERSITY OF GLASGOW 

 Organization address address: University Avenue
city: GLASGOW
postcode: G12 8QQ

contact info
Titolo: Mr.
Nome: Joe
Cognome: Galloway
Email: send email
Telefono: +44 1413303884

 Nazionalità Coordinatore United Kingdom [UK]
 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-2013-CIG
 Funding Scheme MC-CIG
 Anno di inizio 2014
 Periodo (anno-mese-giorno) 2014-03-01   -   2018-02-28

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITY OF GLASGOW

 Organization address address: University Avenue
city: GLASGOW
postcode: G12 8QQ

contact info
Titolo: Mr.
Nome: Joe
Cognome: Galloway
Email: send email
Telefono: +44 1413303884

UK (GLASGOW) coordinator 100˙000.00

Mappa


 Word cloud

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

intracellular    release    cluster    rabbit    cell    ryr    calcium    remodeling    alterations    arrhythmic    electrical    heart    functional    waves   

 Obiettivo del progetto (Objective)

'Contraction of the heart occurs by the intracellular release of calcium through channels called ryanodine receptors (RyR), after electrical activation. Due to the progression of heart disease, structural and functional remodeling of at the level of the cardiac cell is known to occur. This remodeling process alters the electrical properties of the heart muscle cell and can lead to the production of an irregularity in the electrical activity of the heart called an arrhythmia. Studies have shown a that disruption of the normal behavior of the RyR can lead to the production of arrhythmic events and these have been linked to the occurrence of intracellular waves of propagating calcium release called calcium waves. The precise mechanisms which underlie this process are currently unknown and warrant further investigation. Using a multidisciplinary approach, alterations in RyR cluster structure will be assessed and correlated with alterations in calcium release after remodeling in a rabbit model of myocardial infarction. Using cultured rabbit myocytes, the involvement of a protein called junctophilin-2 in the regulation of the RyR clustering process will also be assessed. The functional consequences of RyR cluster morphological alteration will be assessed, such as phosphyorylation and the efficacy of anti-arrhythmic drugs.'

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