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SLC39A9 (ZIP9) Regulates Zinc Homeostasis in the Secretory Pathway: Characterization of the ZIP Subfamily I Protein in Vertebrate Cells
Author(s) -
Wataru Matsuura,
Tomohiro Yamazaki,
Yuko YamaguchiIwai,
Seiji Masuda,
Masaya Nagao,
Glen K. Andrews,
Taiho Kambe
Publication year - 2009
Publication title -
bioscience biotechnology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.509
H-Index - 116
eISSN - 1347-6947
pISSN - 0916-8451
DOI - 10.1271/bbb.80910
Subject(s) - zinc , homeostasis , alkaline phosphatase , biology , subfamily , microbiology and biotechnology , secretion , zinc deficiency (plant disorder) , cytosol , golgi apparatus , biochemistry , enzyme , chemistry , endocrinology , medicine , gene , endoplasmic reticulum , organic chemistry
The SLC39A family of zinc transporters can be divided into four subfamilies (I, II, LIV-1, and gufA) in vertebrates, but studies of their functions have been restricted exclusively to members of subfamilies II and LIV-1. In this study, we characterized SLC39A9 (ZIP9), the only member of subfamily I in vertebrates. Confocal microscopy demonstrated that transiently expressed, HA-tagged human ZIP9 (hZIP9-HA) was localized to the trans-Golgi network regardless of zinc status. Disruption of the ZIP9 gene in DT40 cells did not change the growth rate, sensitivity to high zinc and manganese concentrations during long-term culture, or cellular zinc status after short-term incubation with zinc. The alkaline phosphatase activity of ZIP9(-/-) cells did not change in cells cultured in medium containing normal zinc levels. In contrast, the activity of this enzyme decreased in wild-type cells cultured in zinc deficient medium but less so in ZIP9(-/-) cells under these conditions. Stable over-expression of hZIP9-HA moderately decreased alkaline phophatase activity. These results suggest that ZIP9 functions to regulate zinc homeostasis in the secretory pathway without significantly altering cytosolic zinc homeostasis.

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