CFTR regulation of epithelial sodium channel.

Yawar J. Qadri, Estelle Cormet-Boyaka, Dale J. Benos, Bakhrom K. Berdiev

Research output: Contribution to journalArticlepeer-review

8 Citations (Scopus)

Abstract

Cystic fibrosis (CF) is a lethal genetic disorder, characterized by both clinical and genetic complexities, and arises as a result of mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. The gene encodes a Cl(-) channel belonging to the ABC (ATP Binding Cassette) superfamily of transporters. The members of this superfamily use ATP hydrolysis to fulfill their function as active transporters. So far, CFTR is the only member of this family to function as a cAMP-activated Cl(-) channel. Intense research following the cloning of the CFTR gene has extended the role of the CFTR beyond that of a Cl(-) channel. One of the best recognized, yet still controversial, functions of the CFTR is its ability to modulate the functioning of other transporters. The modulation of epithelial Na(+) channel (ENaC) function serves as a prime example of regulatory function of the CFTR. In this chapter, we will briefly describe an integrated protocol consisting of biochemical and electrophysiological approaches to study the regulation of ENaC by CFTR.

Original languageEnglish
Pages (from-to)35-50
Number of pages16
JournalMethods in molecular biology (Clifton, N.J.)
Volume742
DOIs
Publication statusPublished - 2011

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics

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