a Journal of Postdoctoral Research and Postdoctoral Affairs.
    ISSN : 2328-9791
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Development of a PI3K?-derived peptide as a novel F508del-CFTR potentiator
Author(s) : Ghigo A, Murabito A, Ren K, Pirozzi F, Quinney NL, Caldrer S, Sala V, Laudanna C, Melotti P, Gentzsch M, and Hirsch E
Address : University of Torino, Federico II University, University of North Carolina at Chapel Hill (USA), Universitaria Integrata Verona, Italy.

Background and rationale. The underlying cause of cystic fibrosis (CF) is a mutation in the gene encoding the CF transmembrane conductance regulator (CFTR), a cyclic AMP (cAMP)-stimulated chloride channel. A number of CFTR correctors and potentiators, restoring membrane expression and cAMP-mediated activation of the channel, have been developed, but their efficacy is not fully satisfactory (1, 2).

Hypothesis and objectives. The ultimate goal of this project is to validate a novel therapeutic tool for CF. We recently developed a peptide targeting the kinase-independent function of PI3Kγ (3), which we found involved in the regulation of cAMP-mediated gating of the CFTR. Here, we hypothesize that this molecule could be therapeutically exploited to rescue the conductance of the most prevalent CFTR mutant, F508del-CFTR.


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