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Title: ATP11C mutation is responsible for the defect in phosphatidylserine uptake in UPS-1 cells.
Authors: Takada, Naoto
Takatsu, Hiroyuki
Miyano, Rie
Nakayama, Kazuhisa  kyouindb  KAKEN_id  orcid (unconfirmed)
Shin, Hye-Won  kyouindb  KAKEN_id  orcid (unconfirmed)
Author's alias: 申, 惠媛
Issue Date: Nov-2015
Publisher: American Society for Biochemistry and Molecular Biology
Journal title: Journal of lipid research
Volume: 56
Issue: 11
Start page: 2151
End page: 2157
Abstract: Type IV P-type ATPases (P4-ATPases) translocate phospholipids from the exoplasmic to the cytoplasmic leaflets of cellular membranes. We and others previously showed that ATP11C, a member of the P4-ATPases, translocates phosphatidylserine (PS) at the plasma membrane. Twenty years ago, the UPS-1 (uptake of fluorescent PS analogs) cell line was isolated from mutagenized Chinese hamster ovary (CHO)-K1 cells with a defect in nonendocytic uptake of nitrobenzoxadiazole PS. Due to its defect in PS uptake, the UPS-1 cell line has been used in an assay for PS-flipping activity; however, the gene(s) responsible for the defect have not been identified to date. Here, we found that the mRNA level of ATP11C was dramatically reduced in UPS-1 cells relative to parental CHO-K1 cells. By contrast, the level of ATP11A, another PS-flipping P4-ATPase at the plasma membrane, or CDC50A, which is essential for delivery of most P4-ATPases to the plasma membrane, was not affected in UPS-1 cells. Importantly, we identified a nonsense mutation in the ATP11C gene in UPS-1 cells, indicating that the intact ATP11C protein is not expressed. Moreover, exogenous expression of ATP11C can restore PS uptake in UPS-1 cells. These results indicate that lack of the functional ATP11C protein is responsible for the defect in PS uptake in UPS-1 cells and ATP11C is crucial for PS flipping in CHO-K1 cells.
Rights: This research was originally published in [The Journal of Lipid Research, 56, 2151-2157. doi: 10.1194/jlr.M062547] © the American Society for Biochemistry and Molecular Biology
This is not the published version. Please cite only the published version. この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。
DOI(Published Version): 10.1194/jlr.M062547
PubMed ID: 26420878
Appears in Collections:Journal Articles

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