Kim, Seong-Seop Bae, Yeonju Kwon, Osung Kwon, Seung-Hae Seo, Jong Bok Hwang, Eun Mi Park, Jae-Yong 2024-01-19T11:01:30Z 2024-01-19T11:01:30Z 2022-11-10 2022-10 https://pubs.kist.re.kr/handle/201004/114458 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 beta-coat protein (COP) regulated the surface expression and activity of the TWIK1/TREK1 heterodimeric channels in astrocytes. beta-COP binds directly to TREK1 but not TWIK1 in a heterologous expression system. However, beta-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 beta-COP is a potential regulator of astrocytic passive conductance in the brain. English Multidisciplinary Digital Publishing Institute (MDPI) β-COP Regulates TWIK1/TREK1 Heterodimeric Channel-Mediated Passive Conductance in Astrocytes Article 10.3390/cells11203322 1 Cells, v.11, no.20 Cells 11 20 Y scie scopus 000872505300001 Cell Biology Cell Biology Article ENDOPLASMIC-RETICULUM SURFACE EXPRESSION PROTEIN TREK-1 TRAFFICKING TRANSPORT RECEPTOR CELLS beta-COP protein-protein interaction TREK1 TWIK1 astrocytes passive conductance