DEPREC

The Dependence Receptors notion: from a cell biology paradigm to anti-cancer targeted therapy

Coordinatore	UNIVERSITE LYON 1 CLAUDE BERNARD    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
Nazionalità Coordinatore	France [FR]
Totale costo	2˙485˙037 €
EC contributo	2˙485˙037 €
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-2011-ADG_20110310
Funding Scheme	ERC-AG
Anno di inizio	2012
Periodo (anno-mese-giorno)	2012-05-01   -   2017-04-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	UNIVERSITE LYON 1 CLAUDE BERNARD  Organization address address: BOULEVARD DU 11 NOVEMBRE 1918 NUM43 city: VILLEURBANNE CEDEX postcode: 69622 contact info Titolo: Dr. Nome: Javier Cognome: Olaiz Email: send email Telefono: 33472697600 Fax: 33472697609	FR (VILLEURBANNE CEDEX)	hostInstitution	2˙485˙037.00
2	UNIVERSITE LYON 1 CLAUDE BERNARD  Organization address address: BOULEVARD DU 11 NOVEMBRE 1918 NUM43 city: VILLEURBANNE CEDEX postcode: 69622 contact info Titolo: Dr. Nome: Patrick Cognome: Mehlen Email: send email Telefono: 33478782870 Fax: 33478782887	FR (VILLEURBANNE CEDEX)	hostInstitution	2˙485˙037.00

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 Obiettivo del progetto (Objective)

'While it is assumed that transmembrane receptors are active only in the presence of ligand, we have proposed that some receptors may also be active in the absence of ligand stimulation. These receptors, named “dependence receptors” (DRs) share the ability to transmit two opposite signals: in the presence of ligand, these receptors transduce various classical “positive” signals, whereas in the absence of ligand, they trigger apoptosis. The expression of dependence receptors thus creates cellular states of dependence for survival on their respective ligands. To date, more than fifteen such receptors have been identified, including the netrin-1 receptors DCC (Deleted in Colorectal Cancer) and UNC5H1-4, some integrins, RET, EPHA4, TrkA, TrkC and the Sonic Hedgehog receptor Patched (Ptc). Even though the interest in this notion is increasing, two main questions remain poorly understood: (i) how very different receptors, with only modest homology, are able to trigger apoptosis when unengaged by their respective ligand, and (ii) what are the respective biological roles of this pro-apoptotic activity in vivo. We have hypothesized that the DRs pro-apoptotic activity is a mechanism that determines and regulates the territories of migration/localization of cells during embryonic development. We also demonstrated that this may be a mechanism that limits tumor growth and metastasis. The goal of the present project is, based on the study of a relatively small number of these receptors –i.e., DCC, UNC5H, RET, TrkC, Ptc- with a specifically larger emphasis on netrin-1 receptors, to address (i) the common and divergent cell signaling mechanisms triggering apoptosis downstream of these receptors and (ii) the physiological and pathological roles of these DRs on development of neoplasia in vivo. This latter goal will allow us to investigate how this pro-apoptotic activity can be of use to improve and diversify alternative anti-cancer therapeutic approaches.'