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  1. 学術雑誌論文
  2. その他
  1. 部局別インデックス
  2. 医学部

A modified version of galectin-9 induces cell cycle arrest and apoptosis of Burkitt and Hodgkin lymphoma cells

http://hdl.handle.net/20.500.12000/10319
http://hdl.handle.net/20.500.12000/10319
d3db9e48-7cea-4c8a-95a1-82439167aff4
名前 / ファイル ライセンス アクション
BJH53.Fig.Final.pdf BJH53.Fig.Final.pdf
BJH53.final.pdf BJH53.final.pdf
Item type デフォルトアイテムタイプ(フル)(1)
公開日 2009-05-28
タイトル
タイトル A modified version of galectin-9 induces cell cycle arrest and apoptosis of Burkitt and Hodgkin lymphoma cells
言語 en
作成者 Makishi, Shoko

× Makishi, Shoko

en Makishi, Shoko

Okudaira, Takeo

× Okudaira, Takeo

en Okudaira, Takeo

Ishikawa, Chie

× Ishikawa, Chie

en Ishikawa, Chie

Sawada, Shigeki

× Sawada, Shigeki

en Sawada, Shigeki

Watanabe, Toshiki

× Watanabe, Toshiki

en Watanabe, Toshiki

Hirashima, Mitsuomi

× Hirashima, Mitsuomi

en Hirashima, Mitsuomi

Sunakawa, Hajime

× Sunakawa, Hajime

en Sunakawa, Hajime

Mori, Naoki

× Mori, Naoki

en Mori, Naoki

アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
主題
言語 ja
主題Scheme Other
主題 NF-κB
内容記述
内容記述タイプ Other
内容記述 Identification of galectin-9 as a ligand for T-cell immunoglobulin- and mucin-domain-containing molecule-3 (Tim-3), expressed on Th1 cells, has established the Tim-3-galectin-9 pathway as a regulator of Th1 immunity. Whereas there is compelling evidence for the effects of galectin-9 on T-cell fate, limited information is available on the impact of galectin-9 on B lymphocytes. We found that protease-resistant galectin-9, hG9NC(null), but not galectin-1 or -8, prevented cell growth of malignant B cells such as Burkitt lymphoma (BL) and Hodgkin lymphoma (HL). β-galactoside binding was essential for galectin-9-induced cell growth suppression. hG9NC(null) induced cell cycle arrest by reducing the expression of cyclin D1, D2, B1, Cdk4, Cdc25C and c-Myc, and apoptosis by reducing the expression of XIAP, c-IAP2 and survivin. Most of these genes are regulated by nuclear factor-κB (NF-κB), and constitutive activation of NF-κB is a common characteristic of both types of malignancies. hG9NC(null) inhibited IκBα phosphorylation, resulting in suppression of NF-κB. AP-1 has also been implicated in the control of cell survival. hG9NC(null) inhibited the expression of JunD, resulting in the suppression of AP-1. Our results suggest that hG9NC(null) is a potentially suitable agent for the management of BL and HL.
内容記述タイプ Other
内容記述 論文
出版者
言語 en
出版者 Blackwell Publishing
言語
言語 eng
資源タイプ
資源タイプ journal article
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
出版タイプ
出版タイプ AM
出版タイプResource http://purl.org/coar/version/c_ab4af688f83e57aa
識別子
識別子 http://hdl.handle.net/20.500.12000/10319
識別子タイプ HDL
関連情報
関連識別子
識別子タイプ URI
関連識別子 http://www3.interscience.wiley.com/journal/120120074/abstract
関連識別子
識別子タイプ DOI
関連識別子 10.1111/j.1365-2141.2008.07229.x
収録物識別子
収録物識別子タイプ ISSN
収録物識別子 0007-1048
収録物識別子タイプ NCID
収録物識別子 AA00574570
収録物名
言語 en
収録物名 British journal of haematology
書誌情報
巻 142, 号 4, p. 583-594
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