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Related Experiment Videos

CFTR!

C M Fuller1, D J Benos

  • 1Department of Physiology and Biophysics, University of Alabama 35294.

The American Journal of Physiology
|August 1, 1992
PubMed
Summary
This summary is machine-generated.

Cystic fibrosis (CF) is a genetic disorder affecting electrolyte transport. This review analyzes the CF transmembrane conductance regulator (CFTR) protein

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Area of Science:

  • Genetics
  • Molecular Biology
  • Physiology

Background:

  • Cystic fibrosis (CF) is a fatal genetic disorder impacting electrolyte transport in secretory epithelia.
  • Defects in cAMP-mediated chloride (Cl-) transport are central to CF pathophysiology.
  • Electrophysiological studies have characterized Cl- channels in CF-affected tissues.

Purpose of the Study:

  • To analyze electrophysiological and biochemical studies on the CF transmembrane conductance regulator (CFTR) protein.
  • To examine structure-function relationships of the CFTR protein in light of current knowledge.
  • To review evidence suggesting CFTR may function as both a pump and a channel.

Main Methods:

  • Review of existing electrophysiological studies on Cl- channels in secretory epithelia.

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  • Analysis of biochemical data concerning CFTR protein structure and function.
  • Integration of findings with current understanding of CFTR gene product function.

    • Main Results:

    • CFTR protein, a member of ATP-binding proteins, is implicated in CF.
    • The common delta F508 mutation affects CFTR protein structure.
    • CFTR overexpression leads to cAMP-sensitive Cl- channel activity.

    Conclusions:

    • CFTR protein structure shares similarities with ATP-dependent pumps.
    • Evidence suggests CFTR may function as both a pump and a channel.
    • This dual function aligns with the complex nature of cystic fibrosis.