『徳島大学 教育・研究者情報データベース (EDB)』---[学外] /
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登録内容 (EID=174129)

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種別 (必須): 学術論文 (審査論文) [継承]
言語 (必須): 英語 [継承]
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): 1.大学院ソシオテクノサイエンス研究部.ライフシステム部門 (2006年4月1日〜) [継承]
著者 (必須): 1. (英) Nakatani Masashi (日) (読)
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[継承]
2. (英) Takehara Yuka (日) (読)
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[継承]
3. (英) Sugino Hiromu (日) (読)
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[継承]
4.松本 満 ([徳島大学.先端酵素学研究所.重点研究部門])
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[継承]
5. (英) Hashimoto Osamu (日) (読)
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[継承]
6. (英) Hasegawa Yoshihisa (日) (読)
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[継承]
7. (英) Murakami Tatsuya (日) (読)
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8. (英) Uezumi Akiyoshi (日) (読)
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9. (英) Takeda Shin'ichi (日) (読)
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10.野地 澄晴 ([徳島大学])
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11. (英) Sunada Yoshihide (日) (読)
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12. (英) Tsuchida Kunihiro (日) (読)
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[継承]
題名 (必須): (英) Transgenic expression of a myostatin inhibitor derived from follistatin increases skeletal muscle mass and ameliorates dystrophic pathology in mdx mice.  (日)    [継承]
副題 (任意):
要約 (任意): (英) Myostatin is a potent negative regulator of skeletal muscle growth. Therefore, myostatin inhibition offers a novel therapeutic strategy for muscular dystrophy by restoring skeletal muscle mass and suppressing the progression of muscle degeneration. The known myostatin inhibitors include myostatin propeptide, follistatin, follistatin-related proteins, and myostatin antibodies. Although follistatin shows potent myostatin-inhibiting activities, it also acts as an efficient inhibitor of activins. Because activins are involved in multiple functions in various organs, their blockade by follistatin would affect multiple tissues other than skeletal muscles. In the present study, we report the characterization of a myostatin inhibitor derived from follistatin, which does not affect activin signaling. The dissociation constants (K(d)) of follistatin to activin and myostatin are 1.72 nM and 12.3 nM, respectively. By contrast, the dissociation constants (K(d)) of a follistatin-derived myostatin inhibitor, designated FS I-I, to activin and myostatin are 64.3 microM and 46.8 nM, respectively. Transgenic mice expressing FS I-I, under the control of a skeletal muscle-specific promoter showed increased skeletal muscle mass and strength. Hyperplasia and hypertrophy were both observed. We crossed FS I-I transgenic mice with mdx mice, a model for Duchenne muscular dystrophy. Notably, the skeletal muscles in the mdx/FS I-I mice showed enlargement and reduced cell infiltration. Muscle strength is also recovered in the mdx/FS I-I mice. These results indicate that myostatin blockade by FS I-I has a therapeutic potential for muscular dystrophy.  (日)    [継承]
キーワード (推奨): 1. (英) Animals (日) (読) [継承]
2. (英) Cell Line (日) (読) [継承]
3.フォリスタチン (follistatin) [継承]
4. (英) Gene Expression Regulation (日) (読) [継承]
5. (英) Humans (日) (読) [継承]
6. (英) Kinetics (日) (読) [継承]
7. (英) Mice (日) (読) [継承]
8. (英) Mice, Inbred mdx (日) (読) [継承]
9. (英) Mice, Transgenic (日) (読) [継承]
10. (英) Muscle, Skeletal (日) (読) [継承]
11. (英) Muscular Dystrophies (日) (読) [継承]
12. (英) Mutation (日) (読) [継承]
13. (英) Myostatin (日) (読) [継承]
14. (英) Protein Binding (日) (読) [継承]
15. (英) Transforming Growth Factor beta (日) (読) [継承]
発行所 (推奨):
誌名 (必須): The FASEB journal ([Federation of American Societies for Experimental Biology])
(pISSN: 0892-6638, eISSN: 1530-6860)

ISSN (任意): 1530-6860
ISSN: 0892-6638 (pISSN: 0892-6638, eISSN: 1530-6860)
Title: FASEB journal : official publication of the Federation of American Societies for Experimental Biology
Title(ISO): FASEB J
Supplier: Federation of American Societies for Experimental Biology
Publisher: Federation of American Societies for Experimental Biology
 (NLM Catalog  (Wiley  (Scopus  (CrossRef (Scopus information is found. [need login])
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(必須): 477 487 [継承]
都市 (任意):
年月日 (必須): 西暦 2008年 2月 初日 (平成 20年 2月 初日) [継承]
URL (任意):
DOI (任意): 10.1096/fj.07-8673com    (→Scopusで検索) [継承]
PMID (任意): 17893249    (→Scopusで検索) [継承]
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備考 (任意): 1.(英) Article.Affiliation: Division for Therapies Against Intractable Diseases, Institute for Comprehensive Medical Sciences (ICMS), Fujita Health University, Toyoake, Aichi 470-1192, Japan.  (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]

標準的な表示

和文冊子 ● Masashi Nakatani, Yuka Takehara, Hiromu Sugino, Mitsuru Matsumoto, Osamu Hashimoto, Yoshihisa Hasegawa, Tatsuya Murakami, Akiyoshi Uezumi, Shin'ichi Takeda, Sumihare Noji, Yoshihide Sunada and Kunihiro Tsuchida : Transgenic expression of a myostatin inhibitor derived from follistatin increases skeletal muscle mass and ameliorates dystrophic pathology in mdx mice., The FASEB journal, Vol.22, No.2, 477-487, 2008.
欧文冊子 ● Masashi Nakatani, Yuka Takehara, Hiromu Sugino, Mitsuru Matsumoto, Osamu Hashimoto, Yoshihisa Hasegawa, Tatsuya Murakami, Akiyoshi Uezumi, Shin'ichi Takeda, Sumihare Noji, Yoshihide Sunada and Kunihiro Tsuchida : Transgenic expression of a myostatin inhibitor derived from follistatin increases skeletal muscle mass and ameliorates dystrophic pathology in mdx mice., The FASEB journal, Vol.22, No.2, 477-487, 2008.

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