| Project/Area Number |
61480131
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Tokushima Univ. (1988)
Kumamoto University (1986-1987) |
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Principal Investigator |
EBINA Yousuke Tokushima Univ. Professor, 酵素科学研究センター, 教授 (00112227)
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| Co-Investigator(Kenkyū-buntansha) |
TAKIGUCHI Masaki Kumamoto Univ. Assistant Professor, 医学部, 講師 (40179578)
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| Project Period (FY) |
1986 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥6,200,000 (Direct Cost: ¥6,200,000)
Fiscal Year 1988: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1987: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1986: ¥3,200,000 (Direct Cost: ¥3,200,000)
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| Keywords | Human insulin receptor gene / Regulation of the gene expression / 糖尿病 / プロモーター / インスリン受容体 / チロシンキナーゼ / インスリン作用機構 / インスリン受容体遺伝子 / site directed mutagenesis |
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| Research Abstract |
1. Analysis of the structure-function relationship of the human insulin receptor and its abnormality in Diabetes mellitus. We have already reported that the primary structure of the human insulin receptor and that the tyrosine kinase of the subunit of its receptor is essential for insulin signal transduction. We new report a patient with insulin resistant diabetes who has a deletion of a large part of the tyrosine kinase domain in one allele of the insulin receptor gene. This syndrome was transmitted from mother to daughter, with apparently autosomal dominant trait.
2. Regulation of the gene expression of the human insulin receptor gene. We have already reported that the promoter structure of the human insulin receptor gene and that the four G-C boxes which are located at -600 bp stimulate the transcription 10 times. We have identified the binding of the Sp1 transcription activating factor to these G-C boxes.
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