Molecular mechanisms underlying PKC phosphorylation enhancing and permissive effect on the CFTR chloride channel activity

Cystic Fibrosis is the most common genetic disease in European and North American populations. Chronic bacterial infections and inflammations severely damage the airway system and other exocrine organs such as the pancreas and the intestine. CF is the consequence of mutations in the CFTR gene that conduct to the absence or dysfunction of an essential epithelial protein: the CFTR chloride channel. It is then crucial to understand how the CFTR protein is regulated and modulates the activity of other important epithelial proteins to maintain healthy functional epitheliums. Research conducted in my laboratory focus on the understanding of the molecular mechanisms that underlie CFTR activity. This knowledge is then used to better understand the consequences of mutations in this protein, an essential part of the development of new therapeutic strategies and molecules to correct CFTR dysfunctions.