| ○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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| ○招待 (推奨): |
| ○審査 (推奨): |
| ○カテゴリ (推奨): |
| ○共著種別 (推奨): |
| ○学究種別 (推奨): |
| ○組織 (推奨): |
| ○著者 (必須): | 1. | (英) Nakao Reiko (日) (読)
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| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
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| 2. | 平坂 勝也
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| ○貢献度 (任意): |
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| 3. | (英) Goto Jumpei (日) (読)
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| ○貢献度 (任意): |
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| 4. | (英) Ishidoh Kazumi (日) (読)
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| 5. | (英) Yamada Chiharu (日) (読)
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| 6. | (英) Ohno Ayako (日) (読)
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| 7. | 奥村 裕司
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| [継承] |
| 8. | (英) Nonaka Ikuya (日) (読)
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| [継承] |
| 9. | 安友 康二 ([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.病理系.生体防御医学])
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| 10. | (英) Baldwin KM (日) (読)
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| 11. | (英) Kominami Eiki (日) (読)
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| [継承] |
| 12. | (英) Higashibata Akira (日) (読)
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| ○貢献度 (任意): |
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| [継承] |
| 13. | (英) Nagano Keisuke (日) (読)
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| ○貢献度 (任意): |
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| [継承] |
| 14. | (英) Tanaka Keiji (日) (読)
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| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 15. | 安井 夏生
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| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 16. | (英) Mills EM (日) (読)
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| ○貢献度 (任意): |
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| [継承] |
| 17. | (英) Takeda Shinichi (日) (読)
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| ○貢献度 (任意): |
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| [継承] |
| 18. | 二川 健 ([徳島大学.大学院医歯薬学研究部.医学域.栄養科学部門.医科栄養学系.生体栄養学])
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| ○題名 (必須): | □ | (英) Ubiquitin ligase Cbl-b is a negative regulator for insulin-like growth factor 1 signaling during muscle atrophy caused by unloading. (日)
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| ○副題 (任意): |
| ○要約 (任意): | □ | (英) Skeletal muscle atrophy caused by unloading is characterized by both decreased responsiveness to myogenic growth factors (e.g., insulin-like growth factor 1 [IGF-1] and insulin) and increased proteolysis. Here, we show that unloading stress resulted in skeletal muscle atrophy through the induction and activation of the ubiquitin ligase Cbl-b. Upon induction, Cbl-b interacted with and degraded the IGF-1 signaling intermediate IRS-1. In turn, the loss of IRS-1 activated the FOXO3-dependent induction of atrogin-1/MAFbx, a dominant mediator of proteolysis in atrophic muscle. Cbl-b-deficient mice were resistant to unloading-induced atrophy and the loss of muscle function. Furthermore, a pentapeptide mimetic of tyrosine(608)-phosphorylated IRS-1 inhibited Cbl-b-mediated IRS-1 ubiquitination and strongly decreased the Cbl-b-mediated induction of atrogin-1/MAFbx. Our results indicate that the Cbl-b-dependent destruction of IRS-1 is a critical dual mediator of both increased protein degradation and reduced protein synthesis observed in unloading-induced muscle atrophy. The inhibition of Cbl-b-mediated ubiquitination may be a new therapeutic strategy for unloading-mediated muscle atrophy. (日)
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| ○キーワード (推奨): | 1. | (英) Adaptor Proteins, Signal Transducing (日) (読)
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| 2. | (英) Amino Acid Sequence (日) (読)
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| 3. | (英) Animals (日) (読)
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| 4. | (英) Cell Line (日) (読)
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| 5. | (英) Forkhead Transcription Factors (日) (読)
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| 6. | (英) Hindlimb Suspension (日) (読)
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| 7. | (英) Humans (日) (読)
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| 8. | (英) Insulin Receptor Substrate Proteins (日) (読)
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| 9. | (英) Insulin-Like Growth Factor I (日) (読)
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| 10. | (英) Male (日) (読)
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| 11. | (英) Mice (日) (読)
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| 12. | (英) Mice, Inbred C57BL (日) (読)
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| 13. | (英) Mice, Knockout (日) (読)
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| 14. | (英) Molecular Sequence Data (日) (読)
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| 15. | (英) Muscle Proteins (日) (読)
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| 16. | (英) Muscle, Skeletal (日) (読)
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| 17. | (英) Muscular Atrophy (日) (読)
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| 18. | (英) Oligopeptides (日) (読)
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| 19. | (英) Proto-Oncogene Proteins c-cbl (日) (読)
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| 20. | (英) Rats (日) (読)
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| 21. | (英) Rats, Sprague-Dawley (日) (読)
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| 22. | (英) SKP Cullin F-Box Protein Ligases (日) (読)
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| 23. | (英) Signal Transduction (日) (読)
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| 24. | (英) Space Flight (日) (読)
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| 25. | (英) Ubiquitin (日) (読)
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| ○発行所 (推奨): |
| ○誌名 (必須): | □ | Molecular and Cellular Biology ([アメリカ微生物学会])
(pISSN: 0270-7306, eISSN: 1098-5549)
| ○ISSN (任意): | □ | 1098-5549
ISSN: 0270-7306
(pISSN: 0270-7306, eISSN: 1098-5549) Title: Molecular and cellular biologyTitle(ISO): Mol Cell BiolPublisher: Taylor & Francis (NLM Catalog)
(Scopus)
(CrossRef)
(Scopus information is found. [need login]) | [継承] |
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| ○巻 (必須): | □ | 29
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| ○号 (必須): | □ | 17
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| ○頁 (必須): | □ | 4798 4811
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| ○都市 (任意): |
| ○年月日 (必須): | □ | 西暦 2009年 9月 初日 (平成 21年 9月 初日)
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| ○URL (任意): |
| ○DOI (任意): | □ | 10.1128/MCB.01347-08 (→Scopusで検索)
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| ○PMID (任意): | □ | 19546233 (→Scopusで検索)
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| ○CRID (任意): |
| ○WOS (任意): | □ | 000268813100018
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| ○Scopus (任意): |
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| ○指導教員 (推奨): |
| ○備考 (任意): | 1. | (英) Article.Affiliation: Department of Nutritional Physiology, Institute of Health Biosciences, University of Tokushima Graduate School, Kuramoto-cho, Tokushima, Japan. (日)
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| 2. | (英) Article.PublicationTypeList.PublicationType: Journal Article (日)
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| 3. | (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't (日)
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| 4. | (英) OtherID: PMC2725709 (日)
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