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

Authors :
Kim SS
Bae Y
Kwon O
Kwon SH
Seo JB
Hwang EM
Park JY
Source :
Cells [Cells] 2022 Oct 21; Vol. 11 (20). Date of Electronic Publication: 2022 Oct 21.
Publication Year :
2022

Abstract

Mature astrocytes are characterized by a K <superscript>+</superscript> conductance (passive conductance) that changes with a constant slope with voltage, which is involved in K <superscript>+</superscript> homeostasis in the brain. Recently, we reported that the tandem of pore domains in a weak inward rectifying K <superscript>+</superscript> channel (TWIK1 or KCNK1) and TWIK-related K <superscript>+</superscript> 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.

Details

Language :
English
ISSN :
2073-4409
Volume :
11
Issue :
20
Database :
MEDLINE
Journal :
Cells
Publication Type :
Academic Journal
Accession number :
36291187
Full Text :
https://doi.org/10.3390/cells11203322