β-COP Regulates TWIK1/TREK1 Heterodimeric Channel-Mediated Passive Conductance in Astrocytes

Seong Seop Kim, Yeonju Bae, Osung Kwon, Seung Hae Kwon, Jong Bok Seo, Eun Mi Hwang, Jae Yong Park

Research output: Contribution to journalArticlepeer-review

Abstract

Mature astrocytes are characterized by a K+ conductance (passive conductance) that changes with a constant slope with voltage, which is involved in K+ homeostasis in the brain. Recently, we reported that the tandem of pore domains in a weak inward rectifying K+ channel (TWIK1 or KCNK1) and TWIK-related K+ channel 1 (TREK1 or KCNK2) form heterodimeric channels that mediate passive conductance in astrocytes. However, little is known about the binding proteins that regulate the function of the TWIK1/TREK1 heterodimeric channels. Here, we found that β-coat protein (COP) regulated the surface expression and activity of the TWIK1/TREK1 heterodimeric channels in astrocytes. β-COP binds directly to TREK1 but not TWIK1 in a heterologous expression system. However, β-COP also interacts with the TWIK1/TREK1 heterodimeric channel in a TREK1 dependent manner and enhances the surface expression of the heterodimeric channel in astrocytes. Consequently, it regulates TWIK1/TREK1 heterodimeric channel-mediated passive conductance in astrocytes in the mouse brain. Taken together, these results suggest that β-COP is a potential regulator of astrocytic passive conductance in the brain.

Original languageEnglish
Article number3322
JournalCells
Volume11
Issue number20
DOIs
Publication statusPublished - 2022 Oct

Keywords

  • astrocytes
  • passive conductance
  • protein–protein interaction
  • TREK1
  • TWIK1
  • β-COP

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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