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CFTR-dependent chloride efflux in cystic fibrosis mononuclear cells is increased by ivacaftor therapy.

Lorenzo GuerraSusanna D'OriaMaria FaviaStefano CastellaniTeresa SantostasiAngela M PolizziMaria A MariggiòCrescenzio GalloValeria CasavolaPasqualina MontemurroGiuseppina LeonettiAntonio MancaMassimo Conese
Published in: Pediatric pulmonology (2017)
In patients with non-G551D mutations, ivacaftor improved both chloride transport in sweat ducts and chloride efflux in MNC, that is, functions directly imputed to CFTR.
Keyphrases
  • cystic fibrosis
  • pseudomonas aeruginosa
  • lung function
  • induced apoptosis
  • cell cycle arrest
  • endoplasmic reticulum stress
  • cell death
  • air pollution
  • mesenchymal stem cells
  • cell therapy
  • pi k akt