THE RET PROTO-ONCOGENE - Ret as dependence receptor involved in apoptosis, neurogenesis and tumorigenesis (LIFE QUALITY) (2001-08-01 - 2005-07-31) (»add to infobox)

Ugo SERRA, Klaus-Dieter DUEFORMANTEL, Bruno ANDRAL, Annick BERTAULT, Carlo CIANI, Vincenzo COVELLI, Paolo GHELARDONI, Domitien DEBOUZIE

ISTITUTO GIANNINA GASLINI (ITC33 - Genova) (Italy), ALBERT-LUDWIGS-UNIVERSITAET FREIBURG (DE131 - Freiburg im Breisgau, Stadtkreis) (Germany), CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE (CNRS) (FR716 - Rhône) (France), INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE (INSERM) (FR101 - Paris) (France), ISTITUTO EUROPEO DI ONCOLOGIA SRL (ITC45 - Milano) (Italy), ITALIAN AGENCY FOR NEW TECHNOLOGY ENERGY AND THE ENVIRONMENT (IT603 - Roma) (Italy), UNIVERSITA DEGLI STUDI DI PISA (IT517 - Pisa) (Italy), UNIVERSITE CLAUDE BERNARD LYON 1 (FR716 - Rhône) (France)

ER is a classic receptor kinase, which, upon ligand binding, transduces a kinase dependent signal allowing the migration of RET-expressing cells towards ligand source. However recent findings show that RET expression induces apoptosis in the absence of ligand. The dependence receptor notion is based on similar observations that the effects of a number of receptors functioning in both nervous system development and tumorigenesis cannot be explained imply by a positive effect of signal transduction induced by ligand binding. Receptors such as neurotrophin receptor p75NTR, the androgen receptor (AR), DCC (Deleted in Colorectal Cancer), and now RET show two distinct forms of signal transduction depending on ligand availability. In the presence of their ligands they transduce a signal for either proliferation or differentiation and in their absence for apoptosis. This project aims at studying the biological role of RET in model systems and in humans.

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