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Targeting PI3K? scaffold function to activate airway CFTR, limit lung inflammation and pr
     
 
Author(s) : Ghigo A, Murabito A, Ren K, Pirozzi F, Ciraolo E, Montresor A, Richter W, Wenzel D, Matthey M, Quinneu NL, Fleischmann B, Gentzsch M, Laudanna C, Hirsch E
Address : University of Torino, Torino, Italy;Federico II University, Naples, Italy; University of South Alabama, Mobile USA; University of Bonn, Germany;University of North Carolina at Chapel Hill, Chapel Hill, USA
Multiple Institutions in collaboration
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Background and Rationale. The underlying cause of cystic fibrosis (CF) is a mutation in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR), a cyclic AMP (cAMP)-stimulated chloride channel. The consequent CFTR dysfunction primarily affects the respiratory system, where the reduced activity of the channel results in obstruction of small airways and, together with airway inflammation and infections, eventually leads to respiratory failure. A number of CFTR correctors and potentiators have been developed, but their ability to rescue the basic defect of CF is still unsatisfactory. 

Hypothesis and Objectives. We previously showed that phosphoinositide 3-kinase γ (PI3K γ) acts as a scaffold protein and negatively regulates cAMP. Here, we hypothesized that targeting PI3K γ scaffold activity enhances cAMP in airway smooth muscle, immune and epithelial cells, leading to concomitant (i) bronchodilation, (ii) anti-inflammatory effects and (iii) CFTR potentiation. 

 

 
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