| Project/Area Number |
63570523
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
内分泌・代謝学
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| Research Institution | Chiba University School of Medicine |
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Principal Investigator |
MAKINO Hideichi Second Department of Internal Medicine, Lecturer, 医学部・第二内科, 講師 (50009578)
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| Co-Investigator(Kenkyū-buntansha) |
EBINA Yousuke Tokushima University, Institute for Enzyme Research, Professor, 酵素科学研究センター, 教授 (00112227)
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| Project Period (FY) |
1988 – 1989
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| Project Status |
Completed (Fiscal Year 1989)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1989: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1988: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Insulin Receptor / Insulin Receptor Gene / Deletion / Insulin Resistance / Diabetes Mellitus / 糖尿病 / インスリンレセプター / インスリンレセプター遺伝子 / インスリンレセプター異常症 / インスリン抵抗性糖尿病 |
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| Research Abstract |
The insulin receptor has an intrinsic tyrosine kinase activity that is essential for signal transduction. A mutant insulin receptor gene lacking almost the entire kinase domain has been identified in an individual with type A insulin resistance and acanthosis nigricans. Insulin binding to the erythrocytes or cultured fibroblasts from this individual was normal. However receptor autophosphorylation and tyrosine kinase activity toward an exogenous substrate were reduced in partially purified insulin receptors from the preband's lymphocytes that had been transformed by Epstein-Barr virus. The insulin resistance associated with this mutated gene was inherited by the proband from her mother as an apparently autosomal dominant trait. Thus a deletion in one allele of the insulin receptor gene may be at least partly responsible for some instances of insulin-resistant diabetes.
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