| Item type |
文献 / Documents(1) |
| 公開日 |
2022-04-13 |
| アクセス権 |
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|
アクセス権 |
open access |
| 資源タイプ |
|
|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
|
資源タイプ |
journal article |
| 出版社版DOI |
|
|
|
識別子タイプ |
DOI |
|
|
関連識別子 |
https://doi.org/10.1111/jdi.12965 |
|
|
言語 |
ja |
|
|
関連名称 |
10.1111/jdi.12965 |
| 出版タイプ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| タイトル |
|
|
タイトル |
Protein kinase C iota facilitates insulin-induced glucose transport by phosphorylation of soluble nSF attachment protein receptor regulator (SNARE) double C2 domain protein b |
|
言語 |
en |
| タイトル別表記 |
|
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その他のタイトル |
aPKC and DOC2b in glucose transport |
|
言語 |
en |
| 著者 |
ノミヤマ, リュウタ
エモト, マサヒロ
フクダ, ナオフミ
マツイ, クミコ
コンドウ, マナブ
坂根, 亜由子
佐々木, 卓也
タニザワ, ユキオ
|
| 抄録 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
Aims/introduction: 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.
Materials and Methods: 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.
Results: 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.
Conclusions: 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. |
|
言語 |
en |
| キーワード |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
Calcium sensor |
| キーワード |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
Glucose transporter 4 |
| キーワード |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
Insulin signal |
| 書誌情報 |
en : Journal of Diabetes Investigation
巻 10,
号 3,
p. 591-601,
発行日 2018-10-27
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| 収録物ID |
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収録物識別子タイプ |
ISSN |
|
収録物識別子 |
20401124 |
| 収録物ID |
|
|
収録物識別子タイプ |
NCID |
|
収録物識別子 |
AA12488319 |
| 出版者 |
|
|
出版者 |
Asian Association for the Study of Diabetes |
|
言語 |
en |
| 出版者 |
|
|
出版者 |
John Wiley & Sons |
|
言語 |
en |
| 権利情報 |
|
|
言語 |
en |
|
権利情報 |
This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. |
| EID |
|
|
識別子 |
381471 |
|
識別子タイプ |
URI |
| 言語 |
|
|
言語 |
eng |
jdi_10_3_591.pdf (1.1 MB)
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