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ASIC2a-dependent increase of ASIC3 surface expression enhances the sustained component of the currents
- ASIC2a-dependent increase of ASIC3 surface expression enhances the sustained component of the currents
- Kweon, HJ[Kweon, Hae-Jin]; Cho, JH[Cho, Jin-Hwa]; Jang, IS[Jang, Il-Sung]; Suh, BC[Suh, Byung-Chang]
- DGIST Authors
- Kweon, HJ[Kweon, Hae-Jin]; Suh, BC[Suh, Byung-Chang]
- Issue Date
- BMB Reports, 49(10), 542-547
- Article Type
- Acid-Sensing Ion Channel; Endoplasmic Reticulum; Heteromeric Assembly; Membrane Protein; Surface Trafficking
- Acid-sensing ion channels (ASICs) are proton-gated cation channels widely expressed in the nervous system. Proton sensing by ASICs has been known to mediate pain, mechanosensation, taste transduction, learning and memory, and fear. In this study, we investigated the differential subcellular localization of ASIC2a and ASIC3 in heterologous expression systems. While ASIC2a targeted the cell surface itself, ASIC3 was mostly accumulated in the ER with partial expression in the plasma membrane. However, when ASIC3 was co-expressed with ASIC2a, its surface expression was markedly increased. By using bimolecular fluorescence complementation (BiFC) assay, we confirmed the heteromeric association between ASIC2a and ASIC3 subunits. In addition, we observed that the ASIC2a-dependent surface trafficking of ASIC3 remarkably enhanced the sustained component of the currents. Our study demonstrates that ASIC2a can increase the membrane conductance sensitivity to protons by facilitating the surface expression of ASIC3 through herteromeric assembly. © 2016 by the The Korean Society for Biochemistry and Molecular Biology.
- Korean Society for Molecular and Cellular Biology
- Related Researcher
Suh, Byung Chang
Molecular mechanisms of epilepsy and sensory pain transmission; Signaling mechanism of ion channel regulation and membrane excitability; 분자전기생리; 간질 및 통증의 분자적 기전 연구
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- Department of Brain and Cognitive SciencesCurrent Lab1. Journal Articles
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