Cystic fibrosis (CF) is due to mutations in the gene coding for the CFTR chloride channel and is characterized by a persistent and ineffective inflammation of the airway. During the inflammatory process, mediators specialized in the resolution of inflammation, called SPM or specialized pro-resolving mediators (lipoxins, resolvins…), are normally produced from lipoxygenase interactions. We previously demonstrated that these SPMs play a central role in the regulation of innate immunity in restoring ion transport dysfunctions in CF airways and are abnormally produced in the airway of patients.
The goal of this project is to identify the cellular and molecular mechanism involved in the defective production of SPM in cystic fibrosis and to test, in particular, the role of the CFTR protein and CFTR mutations on the biosynthesis and activity of lipoxygenases using biochemistry, molecular biology, interactomic and advanced confocal microscopy approaches.
Candidates for this project should have a solid background in cell culture, molecular biology (transfection, real time PCR), biochemistry (Western Blot, co-immunoprecipitation, immunohistochemistry) and confocal microscopy.
Candidates should e-mail their application, including a CV, a letter of motivation and at least two reference letters to:
Valérie Urbach, Institut Necker Enfants Malades, INSERM U1151, Paris, France, email@example.com, tel: +33 (0)6 30 37 59 04