市川　大樹 (イチカワ　ダイジュ)

Ichikawa, Daiju

写真a

所属（所属キャンパス）

薬学部 薬学科 病態生理学講座 （芝共立）

職名

助教
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論文 【 表示 ／ 非表示 】

  • Temperature-modulated cell-separation column using temperature-responsive cationic copolymer hydrogel-modified silica beads

    Nagase K., Inanaga D., Ichikawa D., Mizutani Akimoto A., Hattori Y., Kanazawa H.

    Colloids and Surfaces B: Biointerfaces （Colloids and Surfaces B: Biointerfaces)  178   253 - 262 2019年06月

    ISSN  09277765

    　概要を見る

    © 2019 Elsevier B.V. There is strong demand for cell separation methods that do not decrease cell activity or modify cell surfaces. Here, new temperature-modulated cell-separation columns not requiring cell-surface premodification are described. The columns were packed with temperature-responsive cationic polymer hydrogel-modified silica beads. Poly(N-isopropylacrylamide-co-n-butyl methacrylate-co-N,N-dimethylaminopropyl acrylamide) hydrogels with various cationic moieties were attached to silica-bead surfaces by radical polymerization using N,Nʹ-methylenebisacrylamide as a crosslinking agent. The beads were packed into solid-phase extraction columns, and temperature-dependent cell elution from the columns was found using HL-60 and Jurkat cells. The retention HL-60 and Jurkat cells in columns containing cationic beads at 37 °C was 95.3% to 99.6% and 95.0% to 98.8%, respectively. By contrast, beads without cationic properties exhibited low cell retention (20.6% for HL-60 and 32.5% for Jurkat cells). The cells were mainly retained through both electrostatic and hydrophobic interactions. The retained HL-60 (4.9%) and Jurkat cells (40%) were eluted at 4 °C from the column with a low composition of cationic monomer (DMAPAAm, 1 mol% in copolymer), because the temperature-responsive hydrogels on the beads became hydrophilic, decreasing the hydrophobic interactions between the cells and the beads. A higher number of Jurkat cells than HL-60 cells were eluted because of differences in their electrostatic properties (Jurkat cells: −2.53 mV; HL-60 cells: −20.7 mV). The results indicated that cell retention by the hydrogel-coated beads packed in a solid phase extraction column could be modulated simply by changing the temperature.

  • A phenylphthalimide derivative, TC11, induces apoptosis by degrading MCL1 in multiple myeloma cells

    Ichikawa D., Nakamura M., Murota W., Osawa S., Matsushita M., Yanagawa H., Hattori Y.

    Biochemical and Biophysical Research Communications （Biochemical and Biophysical Research Communications)  2019年

    ISSN  0006291X

    　概要を見る

    © 2019 To date, the prognosis of multiple myeloma (MM) in patients harboring cytogenetic abnormalities (CA) involving t (4; 14) and deletion of chromosome 17 remains poor despite recent advances in drug development that include the use of immunomodulatory drugs (IMiDs) such as lenalidomide for MM. To address this issue, we have developed a novel phenylphthalimide derivative, TC11, that is structurally related to IMiDs. It remains unclear how TC11 induces apoptosis of MM cells with high-risk CA. Here, we show that TC11 does not induce degradation of CRBN's substrates, IKZF1/3 and CK1α, and induces apoptosis of CRBN-silenced MM; this effect was independent of the cereblon (CRBN) pathway, which is involved in the mechanism of action of IMiDs used for the treatment of MM. We also revealed that TC11, in contrast to existing IMiDs, induced degradation of MCL1 and activation of caspase-9. Furthermore, inhibition of CDK1 by CGP74514A prevented TC11-induced MCL1 degradation, caspase-9 activation, and the subsequent apoptotic cell death. We showed that ectopic MCL1 expression rescued apoptosis of MM. These observations suggest that TC11 induces apoptotic death caused by degradation of MCL1 during prolonged mitotic arrest. Therefore, our findings suggest that TC11 is a potential drug candidate for high-risk MM.

  • A novel derivative (GTN024) from a natural product, komaroviquinone, induced the apoptosis of high-risk myeloma cells via reactive oxygen production and ER stress.

    市川 大樹

    Biochem Biophys Res Commun. 505 （ 3 ） 787 - 793 2018年11月

    研究論文（学術雑誌）, 共著, 査読有り

  • Early Generated B-1-Derived B Cells Have the Capacity To Progress To Become Mantle Cell Lymphoma-like Neoplasia in Aged Mice.

    市川 大樹

    J Immunol. 201 （ 2 ） 804 - 813 2018年07月

    研究論文（学術雑誌）, 共著, 査読有り

  • NLR Nod1 signaling promotes survival of BCR-engaged mature B cells through up-regulated Nod1 as a positive outcome.

    市川 大樹

    J Exp Med. 2017年09月

    研究論文（学術雑誌）, 共著, 査読有り

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KOARA（リポジトリ）収録論文等 【 表示 ／ 非表示 】

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総説・解説等 【 表示 ／ 非表示 】

  • T細胞アナジーとE3ユビキチンリガーゼ

    市川 大樹

    臨床免疫・アレルギー科 (科学評論社)  62 ( 4 ) 411 - 417 2014年10月

    総説・解説（学術雑誌）,  ISSN  1881-1930

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研究発表 【 表示 ／ 非表示 】

  • A novel candidate for immunological target in treatment of multiple myeloma.

    Maiko Matsushita, Saku Saito, Kanae Mori, Shinya Yokoe, Daiju Ichikawa, Yutaka Hattori

    An AACR Special Conference on Tumor Immunology and Immunotherapy (Boston Marriott Copley Place,Boston, U.S.A. ) , 2019年11月

  • 骨髄腫細胞においてリプログラミング遺伝子による脱分化が薬剤抵抗性とクローン増殖を増強する

    Hiroki Tsuji, Takumi Futo, Koichi Samata, Tomofumi Yamamoto, Daiju Ichikawa, Maiko Matsushita, Yutaka Hattori

    The 81th Annual Meeting of the Japanese Society of Hematology, 2019年10月, ポスター（一般）

  • 多発性骨髄腫細胞のレナリドミド耐性に関する多様な分子メカニズム

    Takumi Futo, Ryo Uozaki, Takashi Yamaguchi, Tomofumi Yamamoto， Hiroki Tsuji, Koichi Samata, Daiju Ichikawa，Maiko Matsushita, Yutaka Hattori

    The 81th Annual Meeting of the Japanese Society of Hematology, 2019年10月, 口頭（一般）

  • komaroviquinoneという天然物由来の新規化合物がin vivoにおいて抗MM活性を示す

    佐俣光一、岡山幹夫、藤森宏太、山元智史、市川大樹、松下麻衣子、須藤豊、岩崎源司、山田健人、服部豊

    第78回日本癌学会学術総会, 2019年09月, 国立京都国際会館　京都

  • 天然物由来成分komaroviquinone及びその誘導体群はin vivoにおいて抗骨髄腫活性を示す

    佐俣光一、岡山幹夫、藤森宏太、西山沙織、辻宏樹、不藤拓海、市川大樹、松下麻衣子、岩崎源司、須藤豊、山田健人、平尾磨樹、国枝尚子、長田眞、服部豊

    日本薬学会生物系薬学部会第20回Pharmaco-Hematologyシンポジウム (日本薬学会長井記念館 東京) , 2019年06月

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競争的資金等の研究課題 【 表示 ／ 非表示 】

  • LncRNAを標的とした新規薬剤抵抗性造血器腫瘍の克服

    2019年04月
    -
    2022年03月

    文部科学省・日本学術振興会, 科学研究費助成事業, 市川　大樹, 基盤研究（Ｃ）, 補助金,  代表

  • 難治性多発性骨髄腫に対する新規治療標的分子の探索および機序の解明

    2016年04月
    -
    2018年03月

    文部科学省・日本学術振興会, 科学研究費助成事業, 市川　大樹, 若手研究(B), 補助金,  代表

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担当授業科目 【 表示 ／ 非表示 】

  • 疾患分子生物学特論

    2020年度

  • 病態薬物治療学特論

    2020年度

  • 課題研究（病態生理学）

    2020年度

  • 細胞培養・遺伝子実験特別演習

    2020年度

  • 演習（病態生理学）

    2020年度

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