CALMIRS

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

 Coordinatore UNIVERSITEIT MAASTRICHT 

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.

transduction    surprising    coding    clinical    unexpected    microrna    cardiac    micrornas    hypertrophic    genome    signal    cascade    hypertrophy    generation    cellular    therapeutic    pathological    disease    protein    signaling    mechanisms    heart    pathways    rna   

 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.'

Altri progetti dello stesso programma (FP7-IDEAS-ERC)

FLEXOELECTRICITY (2013)

Flexoelectricity

Read More  

STANIB (2009)

"Space, Time and Number In the Brain"

Read More  

LODESTONE (2013)

LODESTONE: Unifying the Radio Spectrum to Map the Magnetic Universe

Read More