Obiettivo The endoplasmic reticulum (ER) is the cell organelle where secretory and membrane proteins are synthesized and folded. The presence of unfolded/misfolded proteins in the ER causes stress to the cell (“ER stress”) and activates the Unfolded Protein Response (UPR), a cellular response to restore homeostasis in the ER. The presence of misfolded proteins and activation of the UPR have been connected with many diseases and pathological conditions. My goal is to elucidate the molecular mechanisms that regulate neuronal degeneration and cell death induced by ER strees, using Drosophila melanogaster as a model system. To achieve this goal, I propose the following specific aims: 1. Analysis of the molecular mechanisms required for induction of cell death in the context of ER stress. 2. The mechanism of induction of cell death by Xbp1spliced 3. Developmental role of the UPR during photoreceptor differentiation. Campo scientifico natural sciencesbiological sciencesbiochemistrybiomoleculesproteinsmedical and health sciencesbasic medicinephysiologyhomeostasis Parole chiave Drosophila ER stress Health sciences Neural degeneration Unfolded Protein Response eye photoreceptor Programma(i) FP7-PEOPLE - Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) Argomento(i) PEOPLE-2007-4-3.IRG - Marie Curie Action: "International Reintegration Grants" Invito a presentare proposte FP7-PEOPLE-IRG-2008 Vedi altri progetti per questo bando Meccanismo di finanziamento MC-IRG - International Re-integration Grants (IRG) Coordinatore INSTITUTO DE TECNOLOGIA QUIMICA E BIOLOGICA - UNIVERSIDADE NOVA DE LISBOA Contributo UE € 100 000,00 Indirizzo Avenida da Republica, Estacao Agronomica Nacional 2784-505 OEIRAS Portogallo Mostra sulla mappa Tipo di attività Higher or Secondary Education Establishments Contatto amministrativo Pedro Domingos (Mr.) Collegamenti Contatta l’organizzazione Opens in new window Costo totale Nessun dato
