Objectif
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.
Champ scientifique
Appel à propositions
Data not availableRégime de financement
CSC - Cost-sharing contractsCoordinateur
16148 GENOVA
Italie