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DEVELOPMENT OF MHV-RESISTANT MOUSE USING RNAi TRAP METHOD

Research Project

Project/Area Number 13558098
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section展開研究
Research Field Laboratory animal science
Research InstitutionKUMAMOTO UNIVERSITY

Principal Investigator

YAMAMURA Kenichi  KUMAMOTO UNIVERSITY, INSITUTE OF MOLECULAR EMBRYOLOGY AND GENETICS, PROFESSOR, 発生医学研究センター, 教授 (90115197)

Co-Investigator(Kenkyū-buntansha) URANO Toru  KUMAMOTO UNIVERSITY, CENTER FOR ANIMAL RESOURCES AND DEVELOPMENT, PROFESSOR, 動物資源開発研究センター, 教授 (90101899)
Project Period (FY) 2001 – 2002
Project Status Completed (Fiscal Year 2002)
Budget Amount *help
¥11,500,000 (Direct Cost: ¥11,500,000)
Fiscal Year 2002: ¥4,400,000 (Direct Cost: ¥4,400,000)
Fiscal Year 2001: ¥7,100,000 (Direct Cost: ¥7,100,000)
KeywordsRNAi / GENE TRAP / マウス肝炎ウイルス / 遺伝子トラップ / 遺伝子置換 / Cre-loxP
Research Abstract

The post-transriptional gene silencing in animals and plants is called RNA interference (RNAi). RNAi is a process in that double-stranded RNA (dsRNA) induces a sequence-dependent degradation of a cognate mRNA. The natural roles of RNAi might induce defense against viral infection and regulation of the expression of cellular genes. Genetic and biological studies revealed that RNAi is a very complex process that involves many different proteins with mostly unidentified functions. It was reported recendy that 21-nucleotide (nt) synthetic small interfering RNAs (siRNAs) and siRNA that were transcribed by U6 or H1 promoter specifically suppressed the expression of endogenous genes in several lines of mammalian cells. These 21-nt siRNA duplexes were able to evade the INF defense system and these findings suggested that RNAi or an RNAi-related system might exist in mammals.
Mouse hepatitis virus (MHV) infection is an important viral infection in contemporary laboratory colonies. Recently, transgenic and knockout mice are frequently exchanged between investigators leading to the high incidence of contamination of MHV across the countries. At present, we do not have effective methods to prevent infection, nor do we have any treatment. One way to prevent infection is to produce a MHV-resistant mouse. For this purpose, we tried to develop an RNAi gene trap method. We previouly succeeded to develop an exchangeable gene trap method. Using this method, we can carry out a large scale mutagenesis in mice. If we can produce a gene trap mouse which is resistant to MHV at the same time, it will be quite helpful to distribute these mice. However, the method we developed is not still effective to prevent RNA gene expression. Further studies will be required to accomplish the initial purpose.

Report

(3 results)
  • 2002 Annual Research Report   Final Research Report Summary
  • 2001 Annual Research Report
  • Research Products

    (13 results)

All Other

All Publications (13 results)

  • [Publications] Li, Z.-Z., et al.: "Expression of Hqk encoding a KH RNA binding protein is altered in human glioma"Jpn.J.Cancer Res.. 93. 167-177 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Kawazoe, Y., et al.: "Region specific gastrointestinal Hox code during embryonal gut development"Dev Growth Diff.. 44. 77-84 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Araki, K., et al.: "Site-directed integration of the cre gene mediated by Cre recombinase using a combination of mutant lox sites"Nucleic Acid Res. 30. e103-1-e103-8 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Noguchi, H., et al.: "Naso-maxillary deformity due to frontonasal expression of human transthyretin gene in transgenic mice"Genes Cell. 7. 1087-1098 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Li et al.: "Expression of Hqk encoding a KH RNA binding protein is altered in human glioma."Jpn. J. Cancer Res.. 93. 167-177 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Kawazoe et al.: "Region specific gastrointestinal Hox code during embryonal gut development."Dev Growth Diff.. 44. 77-84 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Araki et al.: "Site-directed integration of the cre gene mediated by Cre recombinase using a combination of mutant lox sites."Nucleic Acid Re. 30:e108. 1-8 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Noguchi, H. et al.: "Naso-maxillary deformity due to frontonasal expression of human transthyretin gene in transgenic mice."Genes Cell. 7. 1087-1098 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Li, Z.-Z.et al.: "Expression of Hqk encoding a KH RNA binding protein is altered in human glioma"Jpn.J.Cancer Res.. 93. 167-177 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Kawazoe, Y. et al.: "Region specific gastrointestinal Hox code during embryonal gut development"Dev Growth Duff.. 44. 77-84 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Ogawa, M. et al.: "The lacZ gene under the control of the 7kb of human dystrophin muscle specific promoter is expressed in cardiac muscle but not in adult skeletal muscle in transgenic mice"Neuromuscular Disorders. 11. 244-250 (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] Hoshino, T. et al.: "IL-18 transgenic mice : in vivo evidence of a broad role for IL-18 in modulating immune function"J. Immunol. 14. 7014-7018 (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] Toda, K. et al.: "Targeted disruption of the aromatase P450 gene (Cyp19) in mice and their ovarian and uterine response to 17 -oestradiol"J. Endocrinol. 170. 99-111 (2001)

    • Related Report
      2001 Annual Research Report

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Published: 2001-04-01   Modified: 2016-04-21  

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