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Your search keyword '"Bae, Yeonju"' showing total 19 results
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19 results on '"Bae, Yeonju"'

16. Suppression of 14-3-3γ-mediated surface expression of ANO1 inhibits cancer progression of glioblastoma cells

Author

Lee, Young-Sun, primary, Lee, Jae Kwang, additional, Bae, Yeonju, additional, Lee, Bok-Soon, additional, Kim, Eunju, additional, Cho, Chang-Hoon, additional, Ryoo, Kanghyun, additional, Yoo, Jiyun, additional, Kim, Chul-Ho, additional, Yi, Gwan-Su, additional, Lee, Seok-Geun, additional, Lee, C. Justin, additional, Kang, Sang Soo, additional, Hwang, Eun Mi, additional, and Park, Jae-Yong, additional

Published
2016
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18. Astrocytic NHERF-1 Increases Seizure Susceptibility by Inhibiting Surface Expression of TREK-1.

Author

Bae Y, Lee S, Kim A, Lee S, Kim SS, Park S, Noh J, Ryoo K, Yi GS, Park JY, and Hwang EM

Abstract

Mature hippocampal astrocytes exhibit a linear current-to-voltage (I-V) K + membrane conductance called passive conductance. It is estimated to enable astrocytes to keep potassium homeostasis in the brain. We previously reported that the TWIK-1/TREK-1 heterodimeric channels are crucial for astrocytic passive conductance. However, the regulatory mechanism of these channels by other binding proteins remains elusive. Here, we identified Na+/H+ exchange regulator-1 (NHERF-1), a protein highly expressed in astrocytes, as a novel interaction partner for these channels. NHERF-1 endogenously bound to TWIK-1/TREK-1 in hippocampal cultured astrocytes. When NHERF-1 is overexpressed or silenced, surface expression and activity of TWIK-1/TREK-1 heterodimeric channels are inhibited or enhanced, respectively. Furthermore, we confirmed that reduced astrocytic passive conductance by NHERF-1 overexpressing in the hippocampus increases kainic acid (KA)-induced seizure sensitivity. Taken together, these results suggest that NHERF-1 is a key regulator of TWIK-1/TREK-1 heterodimeric channels in astrocytes and suppression of TREK-1 surface expression by NHERF-1 increases KA-induced seizure susceptibility via reduction of astrocytic passive conductance., (© 2024 The Author(s). GLIA published by Wiley Periodicals LLC.)

Published
2024
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19. A disulphide-linked heterodimer of TWIK-1 and TREK-1 mediates passive conductance in astrocytes.

Author

Hwang EM, Kim E, Yarishkin O, Woo DH, Han KS, Park N, Bae Y, Woo J, Kim D, Park M, Lee CJ, and Park JY

Subjects
Animals, COS Cells, Chlorocebus aethiops, Dimerization, Female, Glutamic Acid metabolism, HEK293 Cells, Humans, Male, Mice, Inbred C57BL, Potassium metabolism, Receptor, Cannabinoid, CB1, Astrocytes metabolism, Potassium Channels, Tandem Pore Domain metabolism
Abstract

TWIK-1 is a member of the two-pore domain K(+) (K2P) channel family that plays an essential part in the regulation of resting membrane potential and cellular excitability. The physiological role of TWIK-1 has remained enigmatic because functional expression of TWIK-1 channels is elusive. Here we report that native TWIK-1 forms a functional channel at the plasma membrane of astrocytes. A search for TWIK-1-binding proteins led to the identification of TREK-1, another member of the K2P family. The TWIK-1/TREK-1 heterodimeric channel is formed via a disulphide bridge between residue C69 in TWIK-1 and C93 in TREK-1. Gene silencing demonstrates that surface expression of TWIK-1 and TREK-1 are interdependent. TWIK-1/TREK-1 heterodimers mediate astrocytic passive conductance and cannabinoid-induced glutamate release from astrocytes. Our study sheds new light on the diversity of K2P channels.

Published
2014
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