| Project/Area Number |
02404030
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Experimental pathology
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| Research Institution | Osaka University |
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Principal Investigator |
KITAMURA Yukihiko Osaka Univ Med Sch Professor, 医学部, 教授 (70028520)
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| Co-Investigator(Kenkyū-buntansha) |
ONOUE Hitoshi Osaka Univ Med Sch Instructor, 医学部, 助手 (70221166)
TSUJIMURA Tohru Osaka Univ Med Sch Instructor, 医学部, 助手 (20227408)
KASUGAI Tsutomu Osaka Univ Med Sch Instructor, 医学部, 助手 (80214310)
HIROTA Seiichi Osaka Univ Med Sch Instructor, 医学部, 助手 (50218856)
NOMURA Shintaro Osaka Univ Med Sch Assoc Prof, 医学部, 助教授 (80159087)
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| Project Period (FY) |
1990 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥32,200,000 (Direct Cost: ¥32,200,000)
Fiscal Year 1993: ¥7,200,000 (Direct Cost: ¥7,200,000)
Fiscal Year 1992: ¥6,100,000 (Direct Cost: ¥6,100,000)
Fiscal Year 1991: ¥6,000,000 (Direct Cost: ¥6,000,000)
Fiscal Year 1990: ¥12,900,000 (Direct Cost: ¥12,900,000)
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| Keywords | Mast Cell / Stem Cell Factor / W locus of mice / Ws locus of rats / Receptor Tyrosine Kinase / Mast Cell-Deficeint Animals / Mast Cell-Deficient Mouse / Mast Cell-Deficient Rat / stem cell factor / レセプタータイロシンキナーゼ / マスト細胞腫 / 好塩基球 / レセプター・タイロンシンカイネース / マスト細胞欠接ラット / cーkitレセプタ- / cーkitレセプタ-のリガンド / 接着因子 / マスト細胞増殖因子 / CーKit遺伝子 / Sl遺伝子座 / 線維芽細胞 |
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| Research Abstract |
Fibroblast-dependent proliferation of mast cells is mediated by stem cell factor (SCF) produced by fibroblasts and c-kit receptor (KIT) expressed on the surface of mast cells. Ws studied the SCF-KIT system from various viewpoints and obtained the following results. 1). Although many KIT mutants have been found in mice, KIT mutants were not known in rats. We described the first KIT mutants in rats. We characterized the Ws (White spotting) locus of rats which encoded the KIT.2). We compared the molecular nature of murine KIT mutants with the number of mast cells in thier skin. 3). We studied the unique KIT mutation designated as Wsh. Although the Wsh mutant allele is located at the W locus, we could not find any abnormalities in the coding region of KIT gene. Since KIT was not transcribed in cultured mast cells derived from the bone marrow of Wsh/Wsh mice, the Wsh mutation was considered to be a mutation at the regulatory region. Since KIT was transcribed in erythroblasts and germ cells of Wsh/Wsh mice, the abnormality of KIT transcription appeared to be cell type specific. Moreover, we found the KIT transcription was influenced by the age in mast cells of Wsh/Wsh mice. Although an appreciable number of mast cells was found in the skin of Wsh/Wsh embryos, mast cells decreased rapidly after birth due to the abolishment of KIT transcription. 4). The mi locus of mice encodes a transcription factor of basic helix-loop-helix leucine zipper family. We demonstrated that the phenotypic abnormalities observed in mast cells of mi/mi mice was attributable to the deficeint transcription of various proteins.
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