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肝疾患におけるIFNλ4の機能的役割の解明
https://doi.org/10.24517/00059151
https://doi.org/10.24517/000591519b895f25-4ab3-4e64-8aae-0143f02f28c4
名前 / ファイル | ライセンス | アクション |
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ME-PR-SHIRASAKI-T-kaken 2019-5p.pdf (83.9 kB)
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Item type | 報告書 / Research Paper(1) | |||||
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公開日 | 2020-10-12 | |||||
タイトル | ||||||
タイトル | 肝疾患におけるIFNλ4の機能的役割の解明 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | Molecular mechanisms and biological, clinical significance of IFNL4 | |||||
言語 | ||||||
言語 | jpn | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_18ws | |||||
資源タイプ | research report | |||||
ID登録 | ||||||
ID登録 | 10.24517/00059151 | |||||
ID登録タイプ | JaLC | |||||
著者別表示 |
Shirasaki, Takayoshi
× Shirasaki, Takayoshi |
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提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 金沢大学医薬保健研究域保健学系 | |||||
書誌情報 |
平成30(2018)年度 科学研究費補助金 若手研究(B) 研究成果報告書 en : 2018 Fiscal Year Final Research Report 巻 2016-04-01 – 2019-03-31, p. 5p., 発行日 2019-05-17 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | iIFNλ4の機能的役割や臨床学的意義について検討した。 (1) 肝動注化学療法奏効例12例の肝組織IFNλ4の発現は非奏効例8例のIFNλ4発現より有意に高発現を示した。(2) IFNλ4は他のIFNとは異なり非常に強い抗腫瘍活性を示すことを明らかにした。また、IFNλ4により特異的に誘導される遺伝子群を同定した。(3) これまでの解析からIFNλ4特異的なレセプターの存在が示唆された。その新規候補レセプターとしてレセプターA及びBが新規レセプターであることを同定した。(4) NOD-SCIDマウスを用いたxenograftモデルにてIFNλ4が抗腫瘍効果を示すことをin vivoで確認した。 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Molecular mechanisms and the biological, clinical significance of IFNλ4 is poorly understood. (1) We examined the expression of IFNλ4 in patients’ samples and evaluated its clinical significance. Hepatic IFNλ4 expression is related to the response to the chemotherapy to advanced HCC. (2) We revealed that IFNλ4 has functional roles quite different from other IFNs. We revealed that IFNλ4 has a strong anti-viral activity and has a strong anti-tumor activity. We identified IFNλ4-dependent gene expression patterns that support the specific phenotype of IFNλ4. (3) We identified new IFNλ4 receptors; A and B. Detailed signaling pathway down streaming of receptor A and B are now under investigating. (4) Anti-tumor activity of IFNλ4 in vivo was evaluated by using xenograft model to NOD-SCID mice. IFNλ4 expressing HepG2 cells established significant small tumors compared to the control tumors or IFNλ3 expressing tumors. |
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内容記述 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 研究課題/領域番号:16K21058, 研究期間(年度):2016-04-01 – 2019-03-31 | |||||
著者版フラグ | ||||||
出版タイプ | AM | |||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/ja/search/?kw=50547180 | |||||
関連名称 | https://kaken.nii.ac.jp/ja/search/?kw=50547180 | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-16K21058/ | |||||
関連名称 | https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-16K21058/ | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-16K21058/16K21058seika/ | |||||
関連名称 | https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-16K21058/16K21058seika/ |