DASPP/BOA PROTEINS

"Functional Analysis of dASPP/Boa, novel regulators of dCsk in epithelial growth and morphogenesis"

Coordinatore	CANCER RESEARCH UK    more  Organization address address: ST JOHN STREET 407 ANGEL BUILDING city: LONDON postcode: EC1V 4AD contact info Titolo: Ms. Nome: Holly Cognome: Elphinstone Email: send email Telefono: +44 207 269 3524 Fax: +44 207 269 3585
Nazionalità Coordinatore	United Kingdom [UK]
Totale costo	171˙300 €
EC contributo	171˙300 €
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-IEF-2008
Funding Scheme	MC-IEF
Anno di inizio	2009
Periodo (anno-mese-giorno)	2009-10-01   -   2011-09-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	CANCER RESEARCH UK  Organization address address: ST JOHN STREET 407 ANGEL BUILDING city: LONDON postcode: EC1V 4AD contact info Titolo: Ms. Nome: Holly Cognome: Elphinstone Email: send email Telefono: +44 207 269 3524 Fax: +44 207 269 3585	UK (LONDON)	coordinator	171˙300.62

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 Obiettivo del progetto (Objective)

'Src-family kinases play major roles in promoting adherens junctions remodelling in development and metastasis. Their activities are negatively regulated by C-terminal Src kinase (Csk). The host lab it has recently shown that Drosophila Ankyrin-repeat, SH3-domain and Proline-rich-region containing (dASPP), together with Boa the homology of mammalian Ras association domain family 8, regulates the function of dCsk in maintaining adherens junctions polarity and integrity in Drosophila (Langton et al., 2007 and unpublished data). However, the molecular nature of this interaction and the exact functions of dASPP and Boa on developing epithelia are still unknown. In this research project, we propose to address the molecular mechanism by which dASPP and Boa regulates dCsk activity and their function in epithelial growth and morphogenesis during development, as well as identify new regulators of Src signalling in epithelial cells.'