SEARCH

a Study of the Epigenetic Alterations that Result in Cardiac Hypertrophy

 Coordinatore THE BABRAHAM INSTITUTE 

 Organization address address: Babraham Hall
city: CAMBRIDGE
postcode: CB22 3AT

contact info
Titolo: Ms.
Nome: Fang
Cognome: Gao
Email: send email
Telefono: -497453
Fax: -497208

 Nazionalità Coordinatore United Kingdom [UK]
 Sito del progetto http://www.ub.edu/searchproject/
 Totale costo 171˙740 €
 EC contributo 171˙740 €
 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) 2010-04-01   -   2012-03-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    THE BABRAHAM INSTITUTE

 Organization address address: Babraham Hall
city: CAMBRIDGE
postcode: CB22 3AT

contact info
Titolo: Ms.
Nome: Fang
Cognome: Gao
Email: send email
Telefono: -497453
Fax: -497208

UK (CAMBRIDGE) coordinator 171˙740.80

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map    transcriptional    hypertrophy    transcription    cardiac    modifications   

 Obiettivo del progetto (Objective)

'Heart failure is a major cause of mortality and morbidity, and often the consequence of pathological cardiac hypertrophy. Upon entering hypertrophy, cells undergo a vast transcriptional remodelling, with thousands of genes being either up- or down-regulated. In the last years it became evident that epigenetic modifications are an important determinant of transcriptional changes, and several lines of evidence demonstrate that epigenome modulating enzymes are implicated in cardiac hypertrophy. In the present project we propose to study transcriptional repression by DNA and histone methylation. We will map these modifications and use this map to identify and study the methyl transferases, transcription factors and pathways that underlie these modifications using a systems-biology approach. The insight that is to be anticipated from this study will not only enhance our understanding of transcription regulation in hypertrophy, it can also provide a novel entry point for strategies to treat this disorder.'

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