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Critical role of the length of the first β strand in insulin receptor kinase activity
https://jichi-ir.repo.nii.ac.jp/records/89
https://jichi-ir.repo.nii.ac.jp/records/89ec7d5a58-5c30-4686-97d2-c10bc32d2117
名前 / ファイル | ライセンス | アクション |
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自治医科大学紀要1881-252X 第38巻 p1-8 2016.3 (501.6 kB)
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Item type | 紀要論文 / Departmental Bulletin Paper(1) | |||||
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公開日 | 2016-06-01 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | Critical role of the length of the first β strand in insulin receptor kinase activity | |||||
その他(別言語等)のタイトル | ||||||
その他のタイトル | インスリン受容体のキナーゼドメインの第1βストランドの長さの重要性 | |||||
言語 | ja | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
言語 | ja | |||||
主題Scheme | Other | |||||
主題 | チロシンキナーゼ | |||||
キーワード | ||||||
言語 | ja | |||||
主題Scheme | Other | |||||
主題 | インスリン受容体 | |||||
キーワード | ||||||
言語 | ja | |||||
主題Scheme | Other | |||||
主題 | 変異 | |||||
キーワード | ||||||
言語 | ja | |||||
主題Scheme | Other | |||||
主題 | インスリン抵抗性 | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | tyrosine kinase | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | insulin receptor | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | mutation | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | insulin resistance | |||||
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 | departmental bulletin paper | |||||
著者 |
Bolormaa, Enkhtuvshin
× Bolormaa, Enkhtuvshin× Tamemoto, Hiroyuki× Nagashima, Shuichi× Bayasgalan, Tumenbayar× Sakai, Kento× Osuga, Jun-ichi× Takahashi, Manabu× Tominaga, Shin-ichi× Ishibashi, Shun |
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著者別名 | ||||||
姓名 | Bolormaa, Enkhtuvshin | |||||
言語 | en | |||||
著者別名 | ||||||
姓名 | 為本, 浩至 | |||||
言語 | ja | |||||
著者別名 | ||||||
姓名 | 永島, 秀一 | |||||
言語 | ja | |||||
著者別名 | ||||||
姓名 | Bayasgalan, Tumenbayar | |||||
言語 | en | |||||
著者別名 | ||||||
姓名 | 坂井, 謙斗 | |||||
言語 | ja | |||||
著者別名 | ||||||
姓名 | 大須賀, 淳一 | |||||
言語 | ja | |||||
著者別名 | ||||||
姓名 | 高橋, 学 | |||||
言語 | ja | |||||
著者別名 | ||||||
姓名 | 富永, 眞一 | |||||
言語 | ja | |||||
著者別名 | ||||||
姓名 | 石橋, 俊 | |||||
言語 | ja | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Background Mutations in the tyrosine kinase domain of the insulin receptor gene cause a monogenic syndrome of insulin resistance in humans. The first β strand in this kinase domain is close to the nucleotide binding loop, and its length is conserved through several species. To test whether the exact length of this region is essential for the kinase activity of the insulin receptor, we constructed a one-amino-acid deletion mutant in the first β strand of the tyrosine kinase domain. Methods Deletion of Arg1000 with concomitant substitution of Glu1001 to Gln (R1000E1001→Q) was generated by sitedirected mutagenesis. Chinese hamster ovary cells were transfected with mutant or wild-type human insulin receptor cDNA, and stable clones with similar binding activity were screened by insulin binding assay and used for further experiments. Receptor expression, kinase activity and downstream insulin signaling were examined by western blot analysis. Results Mature insulin receptor expression was comparable between the wild-type and mutant cells. The mutant insulin receptor showed markedly defective tyrosine kinase activity. Akt kinase phosphorylation was severely reduced, indicating that downstream insulin signaling was also impaired by the mutant receptor. Conclusion This study suggests that the deletion of one residue in the first β strand results in a distortion of the optimal positioning of the kinase structure, thereby compromising the kinase activity of the |
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書誌情報 |
自治医科大学紀要 en : Jichi Medical University Journal 巻 38, p. 1-8, 発行日 2016-03 |
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出版者 | ||||||
出版者 | 自治医科大学 | |||||
ISSN | ||||||
収録物識別子タイプ | PISSN | |||||
収録物識別子 | 1881-252X |