RKTS-33, an Epoxycyclohexenone Derivative That Specifically Inhibits Fas Ligand-Dependent Apoptosis in CTL-Mediated Cytotoxicity
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- 資料種別
- 記事
- 著者・編者
- Tomokazu MitsuiYasunobu MiyakeHideaki Kakeya 他
- タイトル（掲載誌）
- Bioscience, Biotechnology, and Biochemistry
- 巻号年月日等（掲載誌）
- 69(10) (通号 793) 2005.10
- 掲載巻
- 69
- 掲載号
- 10
- 掲載通号
- 793
- 掲載ページ
- 1923～1928
- 掲載年月日（W3CDTF）
- 2005-10
- ISSN（掲載誌）
- 0916-8451
- ISSN-L（掲載誌）
- 0916-8451
- 出版事項（掲載誌）
- Tokyo : Japan Society for Bioscience
- 出版地（国名コード）
- JP
- 本文の言語コード
- eng
- 件名標目
- NDLC
- 対象利用者
- 一般
- 所蔵機関
- 国立国会図書館
- 請求記号
- Z53-G223
- 連携機関・データベース
- 国立国会図書館 : 国立国会図書館雑誌記事索引
- 書誌ID（NDLBibID）
- 7679053
- 整理区分コード
- 632
- 要約等
- Cytotoxic T lymphocytes (CTLs) eliminate virus-infected cells and tumor cells by two distinct killing pathways, mediated by lytic granules containing perforin and by Fas ligand (FasL). ECH [(<I>2R</I>,<I>3R</I>,<I>4S</I>)-2,3-epoxy-4-hydroxy-5-hydroxymethyl-6-(<I>1E</I>)-propenyl-cyclohex-5-en-1-one] has been shown to inhibit FasL-dependent apoptosis or the killing pathway in short-term culture. However, since ECH exhibited cell toxicity in long-term culture, we attempted the synthesis of less toxic epoxycyclohexenone derivatives. In the present study, we found that RKTS-33 [(<I>2R</I>,<I>3R</I>,<I>4S</I>)-2,3-epoxy-4-hydroxy-5-hydroxymethyl-cyclohex-5-en-1-one] has cell toxicity lower than ECH in long-term culture, and further investigated the inhibitory effect of RKTS-33 on CTL-mediated killing pathways. RKTS-33 did not affect cell-surface expression of FasL upon CD3 stimulation, but profoundly inhibited the FasL-dependent killing pathway mediated by CD4<SUP>+</SUP> and CD8<SUP>+</SUP> CTLs, indicating that RKTS-33 specifically blocks target cell apoptosis but not CTL function. By contrast, RKTS-33 did not affect the perforin-dependent killing pathway in CD8<SUP>+</SUP> CTLs. These results indicate that RKTS-33 is a specific inhibitor of the FasL-dependent killing pathway in CTL-mediated cytotoxicity.
- DOI
- 10.1271/bbb.69.1923
- オンライン閲覧公開範囲
- インターネット公開
- 連携機関・データベース
- 科学技術振興機構 : J-STAGE
- 要約等
- Cytotoxic T lymphocytes (CTLs) eliminate virus-infected cells and tumor cells by two distinct killing pathways, mediated by lytic granules containing perforin and by Fas ligand (FasL). ECH [(<I>2R</I>,<I>3R</I>,<I>4S</I>)-2,3-epoxy-4-hydroxy-5-hydroxymethyl-6-(<I>1E</I>)-propenyl-cyclohex-5-en-1-one] has been shown to inhibit FasL-dependent apoptosis or the killing pathway in short-term culture. However, since ECH exhibited cell toxicity in long-term culture, we attempted the synthesis of less toxic epoxycyclohexenone derivatives. In the present study, we found that RKTS-33 [(<I>2R</I>,<I>3R</I>,<I>4S</I>)-2,3-epoxy-4-hydroxy-5-hydroxymethyl-cyclohex-5-en-1-one] has cell toxicity lower than ECH in long-term culture, and further investigated the inhibitory effect of RKTS-33 on CTL-mediated killing pathways. RKTS-33 did not affect cell-surface expression of FasL upon CD3 stimulation, but profoundly inhibited the FasL-dependent killing pathway mediated by CD4<SUP>+</SUP> and CD8<SUP>+</SUP> CTLs, indicating that RKTS-33 specifically blocks target cell apoptosis but not CTL function. By contrast, RKTS-33 did not affect the perforin-dependent killing pathway in CD8<SUP>+</SUP> CTLs. These results indicate that RKTS-33 is a specific inhibitor of the FasL-dependent killing pathway in CTL-mediated cytotoxicity.
- DOI
- 10.1271/bbb.69.1923
- オンライン閲覧公開範囲
- インターネット公開
- 関連情報
- RKTS-33, an epoxycyclohexenone derivative that specifically inhibits Fas ligand-dependent apoptosis in CTL-mediated cytotoxicity
- 関連情報（URI）
- 参照
- A cell-based high-throughput screening method to directly examine transthyretin amyloid fibril formation at neutral pHAn in vitro evaluation of the antioxidant activities of necroptosis and apoptosis inhibitors: the potential of necrostatin-1 and necrostatin-1i to have radical scavenging activities
- 参照
- Concanamycin A, a powerful tool for characterization and estimation of contribution of perforin- and Fas-based lytic pathways in cell-mediated cytotoxicityCytotoxic T lymphocytes: all roads lead to deathConversion of Membrane-bound Fas(CD95) Ligand to Its Soluble Form Is Associated with Downregulation of Its Proapoptotic Activity and Loss of Liver ToxicityHybrid antibodies can target sites for attack by T cellsEpoxycyclohexenone Inhibits Fas-mediated Apoptosis by Blocking Activation of Pro-caspase-8 in the Death-inducing Signaling ComplexNovel non-peptide inhibitors targeting death receptor-Mediated apoptosisApoptosis by Death FactorECH, an Epoxycyclohexenone Derivative That Specifically Inhibits Fas Ligand-Dependent Apoptosis in CTL-Mediated CytotoxicityAntigen-specific directional target cell lysis by perforin-negative T lymphocyte clonesLymphocyte-Mediated CytotoxicityTherapeutic effect of an anti-Fas ligand mAb on lethal graft-versus-host diseaseCD95's deadly mission in the immune systemCytotoxic Cell Granule-Mediated ApoptosisGranzyme B: pro-apoptotic, antiviral and antitumor functionsAntigen presentation by a B-cell line transfected with cloned immunoglobulin heavy- and light-chain genes specific for a defined hapten.Specific suppression of antibody responses by soluble protein‐specific, class II‐restricted cytolytic T lymphocyte clonesFas and its ligand in a general mechanism of T-cell-mediated cytotoxicity.Fas ligand in human serumNuclear war: the granzyme A-bomb
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- 国立情報学研究所 : CiNii Research
- 提供元機関・データベース
- Japan Link Center雑誌記事索引データベースCrossrefPubMedCiNii Articles科学研究費助成事業データベース科学研究費助成事業データベース科学研究費助成事業データベース学術機関リポジトリデータベースCrossrefCrossref
- 書誌ID（NDLBibID）
- 7679053
- NII論文ID
- 130000030524