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 

 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

Mappa


 Word cloud

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cellular    nmii    inflammatory    regulation    cells    regulate    isoforms    cues    inflammation    implicated   

 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.'

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