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Int J Mol Sci. 2017 Aug 14;18(8). pii: E1767. doi: 10.3390/ijms18081767.

The Mechanistic Links between Insulin and Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Cl- Channel.

Author information

1
Department of Molecular Cell Physiology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan. marunaka@koto.kpu-m.ac.jp.
2
Department of Bio-Ionomics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan. marunaka@koto.kpu-m.ac.jp.
3
Japan Institute for Food Education and Health, St. Agnes' University, Kyoto 602-8013, Japan. marunaka@koto.kpu-m.ac.jp.

Abstract

The cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel belongs to the ATP-binding cassette (ABC) transporter superfamily and regulates Cl- secretion in epithelial cells for water secretion. Loss-of-function mutations to the CFTR gene cause dehydrated mucus on the apical side of epithelial cells and increase the susceptibility of bacterial infection, especially in the airway and pulmonary tissues. Therefore, research on the molecular properties of CFTR, such as its gating mechanism and subcellular trafficking, have been intensively pursued. Dysregulated CFTR trafficking is one of the major pathological hallmarks in cystic fibrosis (CF) patients bearing missense mutations in the CFTR gene. Hormones that activate cAMP signaling, such as catecholamine, have been found to regulate the intracellular trafficking of CFTR. Insulin is one of the hormones that regulate cAMP production and promote trafficking of transmembrane proteins to the plasma membrane. The functional interactions between insulin and CFTR have not yet been clearly defined. In this review article, I review the roles of CFTR in epithelial cells, its regulatory role in insulin secretion, and a mechanism of CFTR regulation by insulin.

KEYWORDS:

CFTR; epithelial Cl− transport; insulin

PMID:
28805732
PMCID:
PMC5578156
DOI:
10.3390/ijms18081767
[Indexed for MEDLINE]
Free PMC Article

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