Augmentation of CFTR function in human bronchial epithelial cells via SLC6A14-dependent amino acid uptake: Implications for treatment of Cystic Fibrosis.

CONCLUSION: SLC6A14-mediated L-arginine transport augments residual F508del-CFTR channel function via a non-canonical, NO pathway. This effect is enhanced with increasing pharmacological rescue of F508del-CFTR to the membrane. The current study demonstrates how endogenous pathways can be utilized for the development of companion therapy in CF.
PMID: 31189070 [PubMed - as supplied by publisher]

Source: Mol Biol Cell - June 11, 2019 Category: Molecular Biology Authors: Ahmadi S, Wu YS, Li M, Ip W, Lloyd-Kuzik A, Di Paola M, Du K, Xia S, Lew A, Bozoky Z, Forman-Kay J, Bear CE, Gonska T Tags: Am J Respir Cell Mol Biol Source Type: research