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Indispensable role of Galectin-3 in promoting quiescence of hematopoietic stem cells
https://doi.org/10.24517/00062984
https://doi.org/10.24517/0006298481e63017-0d68-41ca-ab60-47e016ec803f
| 名前 / ファイル | ライセンス | アクション |
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ME-PR-NAITO-H-2118.pdf (5.4 MB)
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| アイテムタイプ | 学術雑誌論文 / Journal Article(1) | |||||||||
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| 公開日 | 2021-07-05 | |||||||||
| タイトル | ||||||||||
| タイトル | Indispensable role of Galectin-3 in promoting quiescence of hematopoietic stem cells | |||||||||
| 言語 | ||||||||||
| 言語 | eng | |||||||||
| 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 | journal article | |||||||||
| ID登録 | ||||||||||
| ID登録 | 10.24517/00062984 | |||||||||
| ID登録タイプ | JaLC | |||||||||
| 著者 |
Jia, Weizhen
× Jia, Weizhen× Kong, Lingyu× Kidoya, Hiroyasu× Naito, Hisamichi× Muramatsu, Fumitaka× Hayashida, Yumiko× Hsieh, Han-Yun× Yamakawa, Daishi× Hsu, Daniel K.× Liu , Fu-Tong× Takakura, Nobuyuki |
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| 著者別表示 |
内藤, 尚道
× 内藤, 尚道
× 高倉, 伸幸
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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医学系 | |||||||||
| 書誌情報 |
Nature Communications 巻 12, 号 1, p. 2118, 発行日 2021-04-09 |
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| ISSN | ||||||||||
| 収録物識別子タイプ | ISSN | |||||||||
| 収録物識別子 | 2041-1723 | |||||||||
| NCID | ||||||||||
| 収録物識別子タイプ | NCID | |||||||||
| 収録物識別子 | AA12645905 | |||||||||
| DOI | ||||||||||
| 関連タイプ | isIdenticalTo | |||||||||
| 識別子タイプ | DOI | |||||||||
| 関連識別子 | 10.1038/s41467-021-22346-2 | |||||||||
| 出版者 | ||||||||||
| 出版者 | Nature Research / Nature Publishing Group | |||||||||
| 抄録 | ||||||||||
| 内容記述タイプ | Abstract | |||||||||
| 内容記述 | Hematopoietic stem cells (HSCs) in adult bone marrow (BM) are usually maintained in a state of quiescence. The cellular mechanism coordinating the balance between HSC quiescence and differentiation is not fully understood. Here, we report that galactose-binding lectin-3 (galectin-3; Gal-3) is upregulated by Tie2 or Mpl activation to maintain quiescence. Conditional overexpression of Gal-3 in mouse HSCs under the transcriptional control of Tie2 or Vav1 promoters (Gal-3 Tg) causes cell cycle retardation via induction of p21. Conversely, the cell cycle of long-term repopulating HSCs (LT-HSCs) in Gal-3-deficient (Gal-3-/-) mice is accelerated, resulting in their exhaustion. Mechanistically, Gal-3 regulates p21 transcription by forming a complex with Sp1, thus blocking cell cycle entry. These results demonstrate that Gal-3 is a negative regulator of cell-cycling in HSCs and plays a crucial role in adult hematopoiesis to prevent HSC exhaustion. © 2021, The Author(s). | |||||||||
| 権利 | ||||||||||
| 権利情報 | copyright © Nature Research | |||||||||
| 著者版フラグ | ||||||||||
| 出版タイプ | VoR | |||||||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||||||
| 関連URI | ||||||||||
| 識別子タイプ | URI | |||||||||
| 関連識別子 | http://www.nature.com/ncomms/index.html | |||||||||
| 関連名称 | http://www.nature.com/ncomms/index.html | |||||||||
| 関連URI | ||||||||||
| 識別子タイプ | URI | |||||||||
| 関連識別子 | https://www.nature.com/articles/s41467-021-22346-2 | |||||||||
| 関連名称 | https://www.nature.com/articles/s41467-021-22346-2 | |||||||||
