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Enhancement of protein productivity of cell by stabilizing mRNA

Research Project

Project/Area Number 03805088
Research Category

Grant-in-Aid for General Scientific Research (C)

Allocation TypeSingle-year Grants
Research Field 化学工学
Research InstitutionUNIVERSITY OF TOKYO

Principal Investigator

SUZUKI Eiji  University of Tokyo, Faculty of Eng., . Associate Professor, 工学部, 助教授 (50226495)

Co-Investigator(Kenkyū-buntansha) KIKUCHI Masako  University of Tokyo, Faculty of Eng., Research Assistant, 工学部(退職), 助手 (60158871)
MAKISHIMA Fusao  University of Tokyo, Faculty of Eng., Lecturer, 工学部, 講師 (30181613)
Project Period (FY) 1991 – 1992
Project Status Completed (Fiscal Year 1992)
Budget Amount *help
¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1992: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1991: ¥1,100,000 (Direct Cost: ¥1,100,000)
KeywordsStability of mRNA / Rate of protein synthesis / Animal cell / Cell culture / Production of protein / Modification of mRNA / Messenger ribonucleic acid / Rate of decomposition / 蛋白質生合成速度 / mRNAの改造 / メッセンジャーリボ核酸の安定性 / メッセンジャ-リボ核酸の安定性
Research Abstract

A structured model predicts that stabilization of mRNA combined with suppression of cell growth enhances the protein production rate of mammalian cells. We confirmed this prediction experimentally as follows.
1. Choosing antibody as an example of ehich the mRNA was stable we confirmed that the mRNA accumulated in cells and the protein production rate per cell increased at the same time as the growth rate of the cells decreased.
3. Addition of caffeine or interleukin 6 into culture medium was the best method to suppress cell growth rate for enhancing the protein productivity.
2. We tried to stabilize mRNA of mouse interleukin 2 which is an example of unstable mRNAs by deleting AU rich region at the 3' untranslated region. Mouse myeloma cells transfected with the modified mRNA produced enhanced amount of the interleukin.

Report

(3 results)
  • 1992 Annual Research Report   Final Research Report Summary
  • 1991 Annual Research Report
  • Research Products

    (8 results)

All Other

All Publications (8 results)

  • [Publications] 鈴木栄二: "細胞増殖抑制によるハイブリドーマの抗体生産性向上 : 最適増殖抑制方法のモデルと実験による探索" 化学工学論文集. 19. 198-206 (1993)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1992 Final Research Report Summary
  • [Publications] 寺田聡: "ハイブリドーマ連続培養の細胞分子生物学的解析とインターロイキン-6を用いたモノクローナル抗体の効率的な生産法" 化学工学論文集. 19. 207-213 (1993)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1992 Final Research Report Summary
  • [Publications] Eiji Suzuki: "Enhanced Antibody Productivity of Hybridomas Due to Growth-Suppression--Experimental and theoretical search for optimal growth-suppression methods--" KAGAKU KOGAKU RONBUNSHU. 19. 198-206 (1993)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1992 Final Research Report Summary
  • [Publications] Satoshi Terada: "Molecular Biological Analysis of Perfusion Culture of Hybridoma and Effective Production of Monoclonal Antibody Using Interleukin-6" KAGAKU KOGAKU RONBUNSHU. 19. 207-213 (1993)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1992 Final Research Report Summary
  • [Publications] 鈴木 栄二: "細胞増殖抑制によるハイブリドーマの抗体生産性向上:最適増殖抑制方法のモデルと実験による探索" 化学工学論文集. (1993)

    • Related Report
      1992 Annual Research Report
  • [Publications] 寺田 聡: "ハイブリドーマ連続培養の細胞分子生物学的解析とインターロイキン-6を用いたモノクローナル抗体の効率的な生産法" 化学工学論文集. (1993)

    • Related Report
      1992 Annual Research Report
  • [Publications] E.Suzuki: "A SIMPEE STRUCTURED MODEL PREDICTED POSITIVELYー,NEGATIVELYOR NONーGROWTH ASSOCIATED ANTIBODY PRODUCTION RATE DEPENDING ON CULTURE CONDITIONS" Proceedings of the Fourth Annual Meeting of Japanese Association for Animal Cell Technology. (1992)

    • Related Report
      1991 Annual Research Report
  • [Publications] Fusao Makishima: "Interleukinー6 is antiproliferative to a mouse hybridoma cell line and promotive for its antibody productivity" Cytotechnology. (1992)

    • Related Report
      1991 Annual Research Report

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Published: 1991-04-01   Modified: 2016-04-21  

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