A Journal of Postdoctoral Research.
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Targeting PI3Ky scaffold function to activate airway CFTR, limit lung inflammation and pr
Hirsch E, Laudanna C, Ghigo A
Centro di Biotecnologie Molecolari
Dip. Biotecnologie Molecolari e Scienze per la Salute, Centro di Biotecnologie Molecolari, Torino; Dip. di Patologia e Diagnostica, Università di Verona, Lab. di Traffico Cellulare e Trasduzione del segnale

Background. 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 ensuing CFTR hypofunction primarily affects the respiratory system, in which the reduced activity of the channel ultimately leads to respiratory failure and death in 80% of CF patients. A number of CFTR correctors and potentiators, restoring membrane expression and cAMP-mediated gating of the channel, have been developed, but their efficacy appears to be unsatisfactory and to strictly rely on elevated concentrations of intracellular cAMP.

Hypothesis and objectives. Given the well-established role of phosphoinositide 3-kinase γ (PI3Kγ) as negative regulator of cAMP, we intend to explore the therapeutic potential of PI3Kγ inhibition in cell-based and pre-clinical models of CF.


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