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Related Experiment Videos

G-proteins modulate amiloride-sensitive sodium channels

J K Bubien1, R S Jope, D G Warnock

  • 1Department of Medicine, University of Alabama at Birmingham 35294.

The Journal of Biological Chemistry
|July 8, 1994
PubMed
Summary
This summary is machine-generated.

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Human B lymphoid cells

Area of Science:

  • Cellular physiology
  • Ion channel regulation
  • Signal transduction

Background:

  • Amiloride-sensitive sodium channels are crucial for cellular function.
  • Their regulation in human B lymphoid cells is not fully understood.
  • G-protein coupled receptors and cyclic AMP pathways are known modulators of ion channels.

Purpose of the Study:

  • To investigate the regulatory mechanisms of amiloride-sensitive sodium conductance in human B lymphoid cells.
  • To elucidate the roles of cyclic adenylyl monophosphate (cAMP) and pertussis toxin-sensitive G-proteins in channel activity.
  • To determine if these pathways act independently or converge on the same sodium channels.

Main Methods:

  • Utilized human B lymphoid cells.
  • Applied cholera toxin to increase cellular cAMP levels.

Related Experiment Videos

  • Used pertussis toxin to ADP-ribosylate GTP-binding proteins.
  • Administered 8-chlorophenylthio-cAMP to modulate cAMP levels.
  • Measured amiloride-sensitive sodium conductance.

    • Main Results:

    • Both cholera toxin and pertussis toxin independently increased amiloride-sensitive sodium conductance.
    • Simultaneous treatment with both toxins did not result in additive increases, suggesting a shared regulatory target.
    • Pre-activation with pertussis toxin followed by cAMP stimulation inhibited the conductance, indicating a dual role for cAMP.
    • Pertussis toxin-sensitive G-proteins can modulate cAMP-mediated regulation of sodium channels.

    Conclusions:

    • Amiloride-sensitive sodium channels in human B lymphoid cells are regulated by at least two independent pathways: one involving cAMP-dependent protein kinase and another involving a pertussis toxin-sensitive G-protein.
    • These pathways converge on the same sodium channels.
    • Cyclic AMP can exert both activating and inhibitory effects on channel activity, depending on the state of G-protein activation.