Understanding the molecular mechanisms that are responsible for ER retention and degradation of CFTR protein (responsible for the genetic disease cystic fibrosis) is the main goal of my research work. Current research interests focus mainly in two different aspects of CFTR biology. 1. Mechanisms of rescue of F508del-CFTR - Understanding how F508del-CFTR is rescued to the cell surface by distinct agents will possibly allow usage of different therapeutic molecules for enhanced results. 2. Elucidating the role of novel CFTR interactors - We are currently interested in clarifying the role of three novel CFTR interactors in the "life-cycle" of CFTR, particularly in its endo/exocytic trafficking, namely: Spleen Tyrosine Kinase (SYK), Lemur Tyrosine Kinase 2 (LMTK2) and Rap1A, a small GTPase, paralogue of Rap1. These advances in CFTR traffic and cell biology, in general, will allow the potential identification of novel therapeutic targets for the treatment of CF patients.