フルテキストURL | A050054000303.pdf ( 495.9KB ) 公開日 2010-04-19
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タイトル | Regulation of insulin signaling via myosin motor protein and actin cytoskeletal network |
作成者 | Nakamori, Yoshitaka
Emoto, Masahiro
Tanizawa, Yukio
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作成者ヨミ | ナカモリ, ヨシタカ
エモト, マサヒロ
タニザワ, ユキオ
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作成者別表記 | 中森, 芳宜
江本, 政広
谷澤, 幸生
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作成者所属 | 山口大学医学部
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内容記述(抄録等) | Impairment of systemic insulin action causes insufficient glucose uptake to cells and compensatory hyper-secretion of insulin from pancreatic β-cells. This insulin-resistant state promotes development of type 2 diabetes, obesity, hypertension, dyslipidemia, and atherosclerosis. Numerous attempts have been made to clarigy this pathogenesis and molocular mechanisms of insulin resistance. Tumor necrosis factor-α(TNF-α) is one of adipocytokines and a major factor causing insulin resistance. This cytokine attenuates insulin signaling by phosphorylation of insulin receptor substrate-1(IRS-1) Ser residues. However little is known about the precise molecular mechanisms. Recently we reported that IκB kinase-β(IKK-β) interacted with IRS-1, and phosphorylated IRS-1 Ser^<307> through molecular motor and actincytoskeleton. In this review, we overview this unique molecular mechanism and propose a new model that molecular motor and cytoskeletal network organize signaling cross-talk.
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本文言語 | eng
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著者キーワード | NEMO
IKK-γ
Myo1c
IRS-1
TNF-α
insulin resistance
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主題 | 医学
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資料タイプ | text |
ファイル形式 | application/pdf |
出版者 | Yamaguchi University School of Medicine
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NII資料タイプ | 紀要論文 |
学内刊行物(紀要等) | The bulletin of the Yamaguchi Medical School |
掲載誌名 | The bulletin of the Yamaguchi Medical School |
巻 | 54 |
号 | 3-4 |
開始ページ | 33 |
終了ページ | 35 |
発行日 | 2007 |
関連情報URL(IsPartOf) | http://ds.cc.yamaguchi-u.ac.jp/~bulletin/index.html
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著者版/出版社版 | 出版社版 |
リポジトリID | A050054000303 |
地域区分 | 山口大学
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URI | http://www.lib.yamaguchi-u.ac.jp/yunoca/handle/A050054000303 |