| ○種別 (必須): | □ | 学術論文 (審査論文)
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| ○言語 (必須): | □ | 英語
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| ○カテゴリ (推奨): |
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| ○学究種別 (推奨): |
| ○組織 (推奨): |
| ○著者 (必須): | 1. | (英) Nomiyama Ryuta (日) (読)
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| 2. | (英) Emoto Masahiro (日) (読)
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| 3. | (英) Fukuda Naofumi (日) (読)
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| 4. | (英) Matsui Kumiko (日) (読)
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| 5. | (英) Kondo Manabu (日) (読)
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| 6. | 坂根 亜由子 ([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.生理系.生化学])
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| 7. | 佐々木 卓也 ([徳島大学.事務局.研究・産学連携部])
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| 8. | (英) Tanizawa Yukio (日) (読)
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| ○題名 (必須): | □ | (英) Protein kinase C iota facilitates insulin-induced glucose transport by phosphorylation of soluble nSF attachment protein receptor regulator (SNARE) double C2 domain protein b. (日)
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| ○要約 (任意): | □ | (英) Double C2 domain protein b (DOC2b), one of the synaptotagmins, has been shown to translocate to the plasma membrane, and to initiate membrane-fusion processes of vesicles containing glucose transporter 4 proteins on insulin stimulation. However, the mechanism by which DOC2b is regulated remains unclear. Herein, we identified the upstream regulatory factors of DOC2b in insulin signal transduction. We also examined the role of DOC2b on systemic homeostasis using DOC2b knockout (KO) mice. We first identified DOC2b binding proteins by immunoprecipitation and mutagenesis experiments. Then, DOC2b KO mice were generated by disrupting the first exon of the DOC2b gene. In addition to the histological examination, glucose metabolism was assessed by measuring parameters on glucose/insulin tolerance tests. Insulin-stimulated glucose uptake was also measured using isolated soleus muscle and epididymal adipose tissue. We identified an isoform of atypical protein kinase C (protein kinase C iota) that can bind to DOC2b and phosphorylates one of the serine residues of DOC2b (S34). This phosphorylation is essential for DOC2b translocation. DOC2b KO mice showed insulin resistance and impaired oral glucose tolerance on insulin and glucose tolerance tests, respectively. Insulin-stimulated glucose uptake was impaired in isolated soleus muscle and epididymal adipose tissues from DOC2b KO mice. We propose a novel insulin signaling mechanism by which protein kinase C iota phosphorylates DOC2b, leading to glucose transporter 4 vesicle translocation, fusion and facilitation of glucose uptake in response to insulin. The present results also showed DOC2b to play important roles in systemic glucose homeostasis. (日)
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| ○キーワード (推奨): | 1. | (英) 3T3-L1 Cells (日) (読)
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| 2. | (英) Adipocytes (日) (読)
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| 3. | (英) Animals (日) (読)
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| 4. | (英) Calcium-Binding Proteins (日) (読)
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| 5. | (英) Cells, Cultured (日) (読)
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| 6. | グルコース (glucose)
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| 7. | (英) Glucose Intolerance (日) (読)
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| 8. | (英) Hypoglycemic Agents (日) (読)
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| 9. | インスリン (insulin)
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| 10. | インスリン抵抗性 (insulin resistance)
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| 11. | (英) Islets of Langerhans (日) (読)
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| 12. | (英) Isoenzymes (日) (読)
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| 13. | 男性 (male)
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| 14. | (英) Mice (日) (読)
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| 15. | (英) Mice, Inbred C57BL (日) (読)
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| 16. | ノックアウトマウス (knockout mice)
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| 17. | (英) Muscle, Skeletal (日) (読)
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| 18. | (英) Nerve Tissue Proteins (日) (読)
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| 19. | リン酸化 (phosphorylation)
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| 20. | (英) Protein Kinase C (日) (読)
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| ○発行所 (推奨): |
| ○誌名 (必須): | □ | Journal of Diabetes Investigation (Asian Association for the Study of Diabetes)
(pISSN: 2040-1116, eISSN: 2040-1124)
| ○ISSN (任意): | □ | 2040-1124
ISSN: 2040-1116
(pISSN: 2040-1116, eISSN: 2040-1124) Title: Journal of diabetes investigationTitle(ISO): J Diabetes InvestigPublisher: John Wiley and Sons Inc (NLM Catalog)
(医中誌Web)
(Scopus)
(CrossRef)
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| ○巻 (必須): | □ | 10
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| ○号 (必須): | □ | 3
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| ○頁 (必須): | □ | 591 601
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| ○都市 (任意): |
| ○年月日 (必須): | □ | 西暦 2019年 5月 初日 (平成 31年 5月 初日)
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| ○URL (任意): |
| ○DOI (任意): | □ | 10.1111/jdi.12965 (→Scopusで検索)
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| ○PMID (任意): | □ | 30369065 (→Scopusで検索)
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| ○CRID (任意): |
| ○WOS (任意): |
| ○Scopus (任意): | □ | 2-s2.0-85057793668
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| ○備考 (任意): | 1. | (英) Article.ELocationID: 10.1111/jdi.12965 (日)
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| 2. | (英) Article.PublicationTypeList.PublicationType: Journal Article (日)
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| 3. | (英) KeywordList.Keyword: Calcium sensor (日)
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| 4. | (英) KeywordList.Keyword: Glucose transporter 4 (日)
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| 5. | (英) KeywordList.Keyword: Insulin signal (日)
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