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Coupling of CFTR Cl- channel gating to an ATP hydrolysis cycle

T Baukrowitz1, T C Hwang, A C Nairn

  • 1Laboratory of Cardiac/Membrane Physiology, Rockefeller University, New York, New York 10021.

Neuron
|March 1, 1994
PubMed

Insights

Cystic fibrosis transmembrane conductance regulator (CFTR) channel opening requires ATP. Inorganic phosphate analogs locked opened CFTR channels, demonstrating that CFTR channel gating is coupled to ATP hydrolysis.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Ion Channel Physiology

Background:

  • Cystic fibrosis transmembrane conductance regulator (CFTR) chloride channels require protein kinase A phosphorylation and nucleoside triphosphate binding for opening.
  • The precise role of ATP hydrolysis in CFTR channel gating remains incompletely understood.

Purpose of the Study:

  • To investigate the direct link between ATP hydrolysis and the opening/closing cycle of CFTR channels.
  • To determine if ATP hydrolysis is a necessary event for CFTR channel gating.

Main Methods:

  • Utilized inside-out patch-clamp electrophysiology on CFTR channels from cardiac myocytes.
  • Applied vanadate (VO4) and beryllium fluoride (BeF3) inorganic phosphate analogs to CFTR channels.
  • These analogs mimic inorganic phosphate, inhibiting ATP hydrolysis by binding to the active site.

Main Results:

  • VO4 and BeF3 analogs were applied to ATP-activated CFTR channels.
  • The analogs locked the CFTR channels in an open state.
  • This resulted in a 2-3 order of magnitude increase in the mean open time of the channels.

Conclusions:

  • CFTR channel opening and closing are intrinsically coupled to the ATP hydrolysis cycle.
  • ATP hydrolysis is essential for the dynamic gating of CFTR channels, not just for initial activation.

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