CALMIRS

RNA-based regulation of signal transduction – Regulation of calcineurin/NFAT signaling by microRNA-based mechanisms

Coordinatore	UNIVERSITEIT MAASTRICHT    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
Nazionalità Coordinatore	Netherlands [NL]
Totale costo	1˙499˙528 €
EC contributo	1˙499˙528 €
Programma	FP7-IDEAS-ERC Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	ERC-2012-StG_20111109
Funding Scheme	ERC-SG
Anno di inizio	2013
Periodo (anno-mese-giorno)	2013-02-01   -   2018-01-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	UNIVERSITEIT MAASTRICHT  Organization address address: Minderbroedersberg 4-6 city: MAASTRICHT postcode: 6200 MD contact info Titolo: Mr. Nome: Rob Cognome: Van Der Zander Email: send email Telefono: +31 43 3881647	NL (MAASTRICHT)	hostInstitution	1˙499˙528.00
2	UNIVERSITEIT MAASTRICHT  Organization address address: Minderbroedersberg 4-6 city: MAASTRICHT postcode: 6200 MD contact info Titolo: Prof. Nome: Leon Johannes Cognome: De Windt Email: send email Telefono: +31 43 3884308 Fax: +31 43 3871055	NL (MAASTRICHT)	hostInstitution	1˙499˙528.00

Mappa

 Word cloud

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

 Obiettivo del progetto (Objective)

'Heart failure is a serious clinical disorder that represents the primary cause of hospitalization and death in Europe and the United States. There is a dire need for new paradigms and therapeutic approaches for treatment of this devastating disease. The heart responds to mechanical load and various extracellular stimuli by hypertrophic growth and sustained pathological hypertrophy is a major clinical predictor of heart failure. A variety of stress-responsive signaling pathways promote cardiac hypertrophy, but the precise mechanisms that link these pathways to cardiac disease are only beginning to be unveiled. Signal transduction is traditionally concentrated on the protein coding part of the genome, but it is now appreciated that the protein coding part of the genome only constitutes 1.5% of the genome. RNA based mechanisms may provide a more complete understanding of the fundamentals of cellular signaling. As a proof-of-principle, we focus on a principal hypertrophic signaling cascade, cardiac calcineurin/NFAT signaling. Here we will establish that microRNAs are intimately interwoven with this signaling cascade, influence signaling strength by unexpected upstream mechanisms. Secondly, we will firmly establish that microRNA target genes critically contribute to genesis of heart failure. Third, the surprising stability of circulating microRNAs has opened the possibility to develop the next generation of biomarkers and provide unexpected mechanisms how genetic information is transported between cells in multicellular organs and fascilitate inter-cellular communication. Finally, microRNA-based therapeutic silencing is remarkably powerful and offers opportunities to specifically intervene in pathological signaling as the next generation heart failure therapeutics. CALMIRS aims to mine the wealth of these RNA mechanisms to enable the development of next generation RNA based signal transduction biology, with surprising new diagnostic and therapeutic opportunities.'