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Related Concept Videos

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Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
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GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
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Related Experiment Video

Updated: May 20, 2026

Monitoring Leucine-Rich Repeat Containing 8 Channel (LRRC8/VRAC) Activity Using Sensitized-Emission Förster Resonance Energy Transfer (SE-FRET)
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Monitoring Leucine-Rich Repeat Containing 8 Channel (LRRC8/VRAC) Activity Using Sensitized-Emission Förster Resonance Energy Transfer (SE-FRET)

Published on: August 9, 2024

Long-chain acylcarnitines regulate the hERG channel.

Fabio Ferro1, Aude Ouillé, Truong-An Tran

  • 1INSERM U921, Université François-Rabelais, Tours, France.

Plos One
|August 1, 2012
PubMed
Summary

Long-chain acyl-carnitines (LCACs) affect cardiac ion channels, potentially explaining arrhythmias in conditions like ischemia. LCACs regulate hERG channel activity, influencing action potential duration and contributing to cardiac arrhythmias.

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Published on: August 9, 2024

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Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology
  • Electrophysiology

Background:

  • Carnitine levels fluctuate in pathological states, linked to cardiac arrhythmias and sudden cardiac death.
  • Acyl-carnitines (acyl-CARs), not carnitine itself, are implicated in ischemia-induced arrhythmias via ion channel modulation.

Purpose of the Study:

  • Investigate the effects of acyl-carnitines on key cardiac ion channels: hERG (IKr), K(IR)2.1 (IK1), and K(v)7.1/minK (IKs).
  • Determine the role of acyl-CARs in modulating ionic currents responsible for cardiac electrical activity.

Main Methods:

  • Utilized patch clamp electrophysiology on HEK293 cells expressing hERG, K(IR)2.1, or Kv7.1/minK channels.
  • Applied various concentrations of free carnitine and medium-chain/long-chain acyl-CARs intracellularly and extracellularly.
  • Included free fatty acids in hERG channel studies.

Main Results:

  • Extracellular long-chain acyl-CARs (LCACs) increased I(hERG) current amplitude and accelerated deactivation kinetics in a dose-dependent manner.
  • No significant effects were observed on K(IR)2.1 or Kv7.1/minK channels.
  • Computer simulations indicated that these changes in I(hERG) affect action potential profiles.

Conclusions:

  • Extracellular LCACs tonically regulate hERG channel amplitude and kinetics under physiological conditions.
  • This modulation by LCACs may contribute to altered action potential duration preceding cardiac arrhythmias.
  • Findings are relevant to understanding arrhythmias in ischemia, diabetes, and primary systemic carnitine deficiency.