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Updated: Feb 2, 2026

Determination of the Relative Cell Surface and Total Expression of Recombinant Ion Channels Using Flow Cytometry
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HAP1 interaction with KCNQ4 attenuates channel surface expression and function.

Jung Ah Kim1, Kyung Seok Oh1, Jae Won Roh1

  • 1Department of Pharmacology, Graduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, Seoul 03722, Republic of Korea.

Molecules and Cells
|January 31, 2026
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Summary

Huntingtin-associated protein 1 (HAP1) negatively regulates the KCNQ4 potassium channel, crucial for hearing. HAP1 reduces KCNQ4 surface expression, impacting inner ear function and offering potential therapeutic targets.

Keywords:
Intracellular traffickingNonsyndromic hearing lossPotassium ion homeostasisProtein-protein interactionVoltage–gated potassium channel

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • KCNQ4 potassium channels are vital for hearing and frequently mutated in hearing loss.
  • The precise interactions and regulatory mechanisms of KCNQ4 remain incompletely understood.

Purpose of the Study:

  • To identify novel KCNQ4 interactors and elucidate their role in KCNQ4 regulation.
  • To investigate the functional impact of HAP1 on KCNQ4 channel activity.

Main Methods:

  • Yeast two-hybrid assay to identify KCNQ4 interactors.
  • Protein domain analysis to determine interaction sites.
  • Biochemical and physiological assays to assess KCNQ4 function and surface expression.

Main Results:

  • Huntingtin-associated protein 1 (HAP1) was identified as a novel interactor of KCNQ4.
  • HAP1 binds to the B-segment of KCNQ4.
  • HAP1 overexpression reduces KCNQ4 surface expression and attenuates potassium currents, indicating negative regulation.

Conclusions:

  • HAP1 acts as a negative regulator of KCNQ4, potentially by disrupting endocytic trafficking.
  • The HAP1-KCNQ4 interaction provides insights into KCNQ4 regulation and suggests a target for hearing loss interventions.