TOR SIGNALLING

Growth control by the TOR signalling network

Coordinatore	UNIVERSITE DE GENEVE    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
Nazionalità Coordinatore	Switzerland [CH]
Totale costo	965˙449 €
EC contributo	965˙449 €
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-2007-StG
Funding Scheme	ERC-SG
Anno di inizio	2008
Periodo (anno-mese-giorno)	2008-09-01   -   2013-08-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	UNIVERSITE DE GENEVE  Organization address address: Rue du General Dufour 24 city: GENEVE postcode: 1211 contact info Titolo: Dr. Nome: Alex Cognome: Waehry Email: send email Telefono: +41 (0)22 379 75 60 Fax: +41 (0)22 379 11 80	CH (GENEVE)	hostInstitution	0.00
2	UNIVERSITE DE GENEVE  Organization address address: Rue du General Dufour 24 city: GENEVE postcode: 1211 contact info Titolo: Prof. Nome: Robbie Joseph Cognome: Loewith Email: send email Telefono: 41 22 379 6116 Fax: -41 22 379 6868	CH (GENEVE)	hostInstitution	0.00

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 Obiettivo del progetto (Objective)

'The Target Of Rapamycin (TOR) kinases reside in two distinct multi-protein complexes: TOR Complex 1 (TORC1), and TORC2. These two complexes are conserved among eukaryotes and function in signalling pathways that regulate different aspects of cell growth. By exploiting the facile genetics of the model eukaryote Saccharomyces cerevisiae, my lab aims to flesh out details of the TOR signalling network with the ultimate goal of understanding how cell, organ and organism growth is regulated. Specifically, the molecular mechanisms that regulate their activity, and the effectors by which TORC1 and TORC2 influence their distal readouts, remain largely unknown. Using both hypothesis-driven approaches and unbiased genetic screens we want to learn how TORC1 activity is regulated by environmental cues and to identify the physiological regulators of TORC2. In addition we will use biochemical approaches to elucidate the signalling mechanisms that couple TORC1 and TORC2 to their downstream effectors/readouts. Lastly, given the conservation of the TOR complexes and their clinical importance, especially in oncology, we will employ both directed chemistry and ‘target-inferred’ high throughput chemical library screens to identify drug-like compounds that inhibit yeast and mammalian TORC1 and TORC2.'