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Author
Fujita, Hirofumi Department of Cytology and Histology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Kaken ID publons researchmap
Bando, Tetsuya Department of Cytology and Histology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Kaken ID researchmap
Oyadomari, Seiichi Division of Molecular Biology, Institute for Genome Research, University of Tokushima
Ochiai, Kazuhiko Department of Basic Science, School of Veterinary Nursing and Technology, Faculty of Veterinary Science, Nippon Veterinary and Life Science University
Watanabe, Masami Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Kumon, Hiromi Innovation Center Okayama for Nanobio-Targeted Therapy, Okayama University
Ohuchi, Hideyo Department of Cytology and Histology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Kaken ID researchmap
Abstract
Dickkopf 3 (Dkk3) is a secreted protein belonging to the Dkk family and encoded by the orthologous gene of REIC. Dkk3/REIC is expressed by mouse and human adrenal glands, but the understanding of its roles in this organ is still limited. To determine the functions of Dkk3 in the mouse adrenal gland, we first identified that the mouse Dkk3 protein is N-glycosylated in the adrenal gland as well as in the brain. We performed proteome analysis on adrenal glands from Dkk3-null mice, in which exons 5 and 6 of the Dkk3 gene are deleted. Twodimensional polyacrylamide gel electrophoresis of adrenal proteins from wild-type and Dkk3-null mice revealed 5 protein spots whose intensities were altered between the 2 genotypes. Mass spectrometry analysis of these spots identified binding immunoglobulin protein (BiP), an endoplasmic reticulum (ER) chaperone. To determine whether mouse Dkk3 is involved in the unfolded protein response (UPR), we carried out a reporter assay using ER-stress responsive elements. Forced expression of Dkk3 resulted in the induction of distinct levels of reporter expression, showing the UPR initiated by the ER membrane proteins of activating transcription factor 6 (ATF6) and inositol-requring enzyme 1 (IRE1). Thus, it is possible that Dkk3 is a physiological ER stressor in the mouse adrenal gland.
Keywords
Dkk3 knockout mouse
adrenal gland
glucose-regulated protein 78
proteome
endoplasmic reticulum stress
Amo Type
Original Article
Published Date
2020-06
Publication Title
Acta Medica Okayama
Volume
volume74
Issue
issue3
Publisher
Okayama University Medical School
Start Page
199
End Page
208
ISSN
0386-300X
NCID
AA00508441
Content Type
Journal Article
language
英語
Copyright Holders
CopyrightⒸ 2020 by Okayama University Medical School
File Version
publisher
Refereed
True
PubMed ID
Web of Science KeyUT
NAID