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PIGA遺伝子変異造血幹細胞の選択的増殖におけるCD109分子とTGF-βの役割
https://doi.org/10.24517/00051613
https://doi.org/10.24517/0005161355ec1138-f1f6-4e76-afaa-ef483687b5c8
名前 / ファイル | ライセンス | アクション |
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HO-PR-YAMAZAKI-H-kaken 2018-4p.pdf (169.1 kB)
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Item type | 報告書 / Research Paper(1) | |||||
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公開日 | 2019-04-19 | |||||
タイトル | ||||||
タイトル | PIGA遺伝子変異造血幹細胞の選択的増殖におけるCD109分子とTGF-βの役割 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | The role of CD109 and TGF-beta for the preferential commitment of PIGA mutant HSPCs in immune-mediated bone marrow failure | |||||
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 | 10.24517/00051613 | |||||
ID登録タイプ | JaLC | |||||
著者 |
山崎, 宏人
× 山崎, 宏人 |
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著者別表示 |
Yamazaki, Hiroto
× Yamazaki, Hiroto |
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提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 金沢大学附属病院輸血部 | |||||
書誌情報 |
平成29(2017)年度 科学研究費補助金 基盤研究(C) 研究成果報告書 en : 2017 Fiscal Year Final Research Report 巻 2015-04-01 - 2018-03-31, p. 4p., 発行日 2018-05-28 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | TGF-β副受容体であるGPIアンカー膜蛋白CD109が、PIGA遺伝子変異造血幹前駆細胞(HSPC)の優先的活性化に関与しているか否かを明らかにするため、白血病細胞株TF-1のCD109をノックアウト(KO)し、野生型との間で、TGF-βに対する感受性を比較した。その結果、CD109KO TF-1細胞では野生型TF-1細胞に比べてTGF-βによるリン酸化SMAD2の誘導が低下し、TGF-βによる細胞増殖の抑制が起こりにくいことが明らかになった。PIGA遺伝子変異HSPCは、TGF-βの作用増強を担うCD109の欠失によりTGF-βによる抑制を免れて造血に寄与しやすくなることが示唆された。 | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | To determine whether a TGF-beta (b) co-receptor CD109 on hematopoietic stem progenitor cells (HSPCs) play a role in the preferential commitment of PIGA mutant HSPCs in patients with immune-mediated bone marrow failure (BMF), we established CD109-knock out (KO) TF-1, a GM-CSF-dependent myeloid leukemia cell line, using the CRIPR/Cas9 system, and compared the sensitivity of CD109KO TF-1 cells to TGF-b to that of wild-type (WT) TF-1 cells. The TGF-b treatment induced pSMAD2 in CD109KO TF-1 cells to a significantly lesser degree than in WT TF-1 cells. The proliferation of CD109KO TF-1 was inhibited by TGF-b also to a lesser degree than WT TF-1 cells. The results suggest that CD109, a glycosylphosphatidylinositol anchor protein, plays an enhancing role in the TGF-b signaling in HSPCs, and the lack of CD109 may make the HSPCs less sensitive to TGF-b, leading to the preferential commitment of the PIGA mutant HSPCs in immune-mediated BMF, in which TGF-b suppresses activation of WT HSPCs. | |||||
内容記述 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 研究課題/領域番号:15K09496, 研究期間(年度):2015-04-01 - 2018-03-31 | |||||
内容記述 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 出典:研究課題「PIGA遺伝子変異造血幹細胞の選択的増殖におけるCD109分子とTGF-βの役割」課題番号15K09496 (KAKEN:科学研究費助成事業データベース(国立情報学研究所)) (https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-15K09496/15K09496seika/)を加工して作成 |
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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/search/?qm=50361994 | |||||
関連名称 | https://kaken.nii.ac.jp/search/?qm=50361994 | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-15K09496/ | |||||
関連名称 | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-15K09496/ | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-15K09496/15K09496seika/ | |||||
関連名称 | https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-15K09496/15K09496seika/ |