『徳島大学 教育・研究者情報データベース (EDB)』---[学外] /
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EID=297022EID:297022, Map:0, LastModified:2015年11月7日(土) 19:42:05, Operator:[大家 隆弘], Avail:TRUE, Censor:0, Owner:[赤松 徹也], Read:継承, Write:継承, Delete:継承.
種別 (必須): 学術論文 (審査論文) [継承]
言語 (必須): 英語 [継承]
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審査 (推奨): Peer Review [継承]
カテゴリ (推奨): 研究 [継承]
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学究種別 (推奨):
組織 (推奨):
著者 (必須): 1.陳 剛
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2.姚 陳娟 ([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.基礎歯学系.口腔分子生理学])
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3.長谷川 敬展 ([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.基礎歯学系.口腔分子生理学])
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4.赤松 徹也 ([徳島大学.大学院社会産業理工学研究部.生物資源産業学域.応用生命系.生体分子機能学分野]/[徳島大学.生物資源産業学部.生物資源産業学科.応用生命講座])
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5.吉村 弘 ([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.基礎歯学系.口腔分子生理学])
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6.細井 和雄
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題名 (必須): (英) Effects of isoproterenol on aquaporin 5 levels in the parotid gland of mice in vivo.  (日)    [継承]
副題 (任意):
要約 (任意): (英) In the membrane fraction of mouse parotid gland (PG), the protein level of aquaporin 5 (AQP5), a member of the water channel family, was increased by injection (ip) of isoproterenol (IPR), a β-adrenergic agonist, at 1 h, and stayed at high levels until 6 h; this change occurred simultaneously as amylase secretion. The AQP5 level then decreased and returned toward the original level at 12-48 h. After IPR injection, the AQP5 mRNA gradually increased and reached a maximum at 24 h. The facts suggest a rapid appearance of AQP5 at plasma membrane by IPR and subsequent degradation/metabolism by activation of proteolytic systems. Pretreatment of animals with two calpain inhibitors, N-Ac-Leu-Leu-methininal (ALLM) and calpeptin, as well as a protein synthesis inhibitor, cycloheximide (CHX), significantly suppressed the IPR-induced AQP5 degradation in the PG membrane fraction; such suppression was not observed by two proteasome inhibitors, MG132 and lactacystin, or the lysosome denaturant chloroquine, although most of these inhibitors increased AQP5 protein levels in unstimulated mice. The AQP5 protein was also degraded by μ-calpain in vitro. Furthermore, we demonstrated that μ-calpain was colocalized with AQP5 in the acinar cells by immunohistochemistry, and its activity in the PG was increased at 6 h after IPR injection. These results suggest that the calpain system was responsible for IPR-induced AQP5 degradation in the parotid gland and that such a system was coupled to the secretory-restoration cycle of amylase in the PG.  (日)    [継承]
キーワード (推奨): 1. (英) aquaporin 5 (日) アクアポリン5 (読) [継承]
2. (英) parotid gland (日) 耳下腺 (読) [継承]
3. (英) isoproterenol (日) イソプロテレノール (読) [継承]
発行所 (推奨):
誌名 (必須): American Journal of Physiology, Endocrinology and Metabolism ([アメリカ生理学会])
(pISSN: 0193-1849, eISSN: 1522-1555)

ISSN (任意): 1522-1555
ISSN: 0193-1849 (pISSN: 0193-1849, eISSN: 1522-1555)
Title: American journal of physiology. Endocrinology and metabolism
Title(ISO): Am J Physiol Endocrinol Metab
Publisher: American Physiological Society
 (NLM Catalog  (Scopus  (CrossRef (Scopus information is found. [need login])
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(必須): 306 [継承]
(必須): 1 [継承]
(必須): E100 E108 [継承]
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年月日 (必須): 西暦 2014年 1月 末日 (平成 26年 1月 末日) [継承]
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DOI (任意): 10.1152/ajpendo.00317.2013    (→Scopusで検索) [継承]
PMID (任意): 24192288    (→Scopusで検索) [継承]
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WOS (任意): 000329193100010 [継承]
Scopus (任意): 2-s2.0-84891527146 [継承]
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備考 (任意): 1.(英) Article.ELocationID: 10.1152/ajpendo.00317.2013  (日)    [継承]
2.(英) Article.PublicationTypeList.PublicationType: Journal Article  (日)    [継承]
3.(英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't  (日)    [継承]
4.(英) OtherID: PMC3920005  (日)    [継承]
5.(英) KeywordList.Keyword: aquaporin 5  (日)    [継承]
6.(英) KeywordList.Keyword: exocytosis  (日)    [継承]
7.(英) KeywordList.Keyword: isoproterenol  (日)    [継承]
8.(英) KeywordList.Keyword: parotid gland  (日)    [継承]
9.(英) KeywordList.Keyword: μ-calpain  (日)    [継承]

標準的な表示

和文冊子 ● Gang Chen, Chenjuan Yao, Takahiro Hasegawa, Tetsuya Akamatsu, Hiroshi Yoshimura and Kazuo Hosoi : Effects of isoproterenol on aquaporin 5 levels in the parotid gland of mice in vivo., American Journal of Physiology, Endocrinology and Metabolism, Vol.306, No.1, E100-E108, 2014.
欧文冊子 ● Gang Chen, Chenjuan Yao, Takahiro Hasegawa, Tetsuya Akamatsu, Hiroshi Yoshimura and Kazuo Hosoi : Effects of isoproterenol on aquaporin 5 levels in the parotid gland of mice in vivo., American Journal of Physiology, Endocrinology and Metabolism, Vol.306, No.1, E100-E108, 2014.

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