MYOII-INFLAM

Non-muscle Myosin II orchestrates the inflammatory response by integrating adhesive and cytokine signaling and the mechanical properties of the inflammatory microenvironment

Coordinatore	UNIVERSIDAD AUTONOMA DE MADRID    more  Organization address address: CALLE EINSTEIN, CIUDAD UNIV CANTOBLANCO RECTORADO 3 city: MADRID postcode: 28049 contact info Titolo: Ms. Nome: Mª Carmen Cognome: Puerta Email: send email Telefono: +34 91 497 8775 Fax: +34 91 497 5269
Nazionalità Coordinatore	Spain [ES]
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	2011
Periodo (anno-mese-giorno)	2011-08-01   -   2015-07-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	UNIVERSIDAD AUTONOMA DE MADRID  Organization address address: CALLE EINSTEIN, CIUDAD UNIV CANTOBLANCO RECTORADO 3 city: MADRID postcode: 28049 contact info Titolo: Ms. Nome: Mª Carmen Cognome: Puerta Email: send email Telefono: +34 91 497 8775 Fax: +34 91 497 5269	ES (MADRID)	coordinator	100˙000.00

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 Obiettivo del progetto (Objective)

'This research aims to understand how inflammatory cues regulate the cellular responses of different cells implicated in inflammation. The main hypothesis is that non-muscle myosin II (NMII) is a central integrator of the different types of extracellular signals produced during the inflammatory response. The precise goal of the present proposal is to understand the regulation and function of the three NMII isoforms in the migration of cells implicated in inflammation, chiefly blood immune cells and cells that drive tissue repair and remodelling (fibroblasts) and vascularization (endothelial cells). This research will address the following objectives: 1) Identify specific kinases, phosphatases and regulatory sites that regulate NMII activation and assembly in a cell type-, stimulus-, isoform- and spatiotemporal-dependent manner. 2) Determine the signalling events and pathways through which the NMII isoforms control the response to inflammatory cues. 3) Elucidate whether the differences in expression and regulation of NMII underlie the different roles of these cells during inflammation. Successful completion of these objectives will provide novel insights on the basic cellular mechanisms of inflammation and bears potential to identify new therapeutic targets.'