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Generation of filggrin-deficient mice and analysis o differentiation and apoptosis of keratinocytes

Research Project

Project/Area Number 11670816
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Dermatology
Research InstitutionGunma University

Principal Investigator

NEGISHI Izumi  Gunma University School of Medicine, assistant professor, 医学部, 講師 (60292611)

Co-Investigator(Kenkyū-buntansha) OHNISHI Kazunori  Gunma University School of Medicine, assistant professor, 医学部, 講師 (60176948)
ISHIKAWA Osamu  Gunma University School of Medicine, professor, 医学部, 教授 (90168188)
Project Period (FY) 1999 – 2001
Project Status Completed (Fiscal Year 2001)
Budget Amount *help
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2001: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2000: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1999: ¥1,500,000 (Direct Cost: ¥1,500,000)
Keywordsfilaggrin / knockout mouse / keratinocyte / apoptosis
Research Abstract

It has been reported that filaggrin may be involved in the terminal differentiation (apoptosis) of keratinocytes. In order to study of keratinocyte differentiation in vivo, we are planning to generate filaggrin-deficient mice. Filaggrin is composed of approximately 320 amino acids and the unit of profilaggrin, which consists of multiple filaggrin-repeats. To generate filaggrin-deficient mice, we need to disrupt the region containing the initiation codon of the profilaggrin gene rather than the coding region of filaggrin. We succeeded to obtain a BAC clone containing the mouse profilaggrin gene with a human profilaggrin cDNA as a probe. We have subloned the important regions of this gene to design a targeting vector. At present, filaggrin^<+/-> ES cells are under construction.

Report

(4 results)
  • 2001 Annual Research Report   Final Research Report Summary
  • 2000 Annual Research Report
  • 1999 Annual Research Report

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Published: 1999-04-01   Modified: 2016-04-21  

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