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Surface expression of the Anoctamin-1 (ANO1) channel is suppressed by protein-protein interactions with beta-COP

Authors
Lee, Young-SunBae, YeonjuPark, NammiYoo, Jae ChealCho, Chang-HoonRyoo, KanghyunHwang, Eun MiPark, Jae-Yong
Issue Date
24-6월-2016
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Keywords
ANO1; beta-COP; Surface expression; Yeast two-hybrid screening; Protein-protein interactions; U251 glioblastoma cells
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.475, no.2, pp.216 - 222
Indexed
SCIE
SCOPUS
Journal Title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume
475
Number
2
Start Page
216
End Page
222
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/88306
DOI
10.1016/j.bbrc.2016.05.077
ISSN
0006-291X
Abstract
Anoctamin-1 (ANO1) is a Ca2+-activated chloride channel (CaCC) that plays important physiological roles in normal and cancerous tissues. However, the plasma membrane trafficking mechanisms of ANO1 remain poorly characterized. In yeast two-hybrid screening experiments, we observed direct interactions of ANO1 with beta-COP, which is a subunit of Coat Protein Complex I (COPI). This interaction was then confirmed using several in vitro and in vivo binding assays. Moreover, the cotransfection of beta-COP with ANO1 into HEK293T cells led to decreased the surface expression and the channel activity of ANO1. Accordingly, endogenous ANO1 was associated with beta-COP in U251 glioblastoma cells, and silencing of beta-COP enhanced surface expression and whole-cell currents of ANO1 in these cells. Taken together, these data suggest that beta-COP negatively regulates ANO1 surface expression. (C) 2016 Elsevier Inc. All rights reserved.
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