| Project/Area Number |
03404065
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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 |
内分泌・代謝学
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| Research Institution | Kyoto University |
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Principal Investigator |
TANAKA Issei (1993) Kyoto University Department of Medicine Lecturer, 医学部, 講師 (80179738)
葛谷 英嗣 (1992) 京都大学, 医学部, 助教授 (20115835)
井村 裕夫 (1991) 京都大学, 医学部, 教授 (10025570)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAMURA Hirotoshi Assistant Professor, 医学部, 助手 (60164331)
NAKAO Kazuwa Kyoto University Department of Medicine Professor, 医学部, 教授 (00172263)
葛谷 英嗣 京都大学, 医学部, 助教授 (20115835)
森 徹 京都大学, 医学部, 教授 (40026894)
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| Project Period (FY) |
1991 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥17,800,000 (Direct Cost: ¥17,800,000)
Fiscal Year 1993: ¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1992: ¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1991: ¥12,600,000 (Direct Cost: ¥12,600,000)
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| Keywords | Insulin Receptor / Insulin Signal Transduction / Natriuretic Peptide Receptors / Endothelin-B Receptor / Thyroid Hormone Receptor / Resistance to Thyroid Hormone / Map Kinase / Point Mutation / インスリン受容体後異常 / 甲状腺ホルモン受容体 / エンドセリン / エンドセリン受容体 / エンドセリン受容体遺伝子 / エンドセリン・レセプタ- / 甲状腺ホルモン・レセプタ- / TSHレセプタ- / バセドウ病 / インスリンレセプタ- |
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| Research Abstract |
Insulin signal transduction. ML-9 (a myosin light chain kinaso inhibitor) inhibited insulin stimulated translocation of glucose transportors (GLUT4 and GLUT1). Insulin stimulated phosphorylation of microtubule-associated protein 2 and myelin basic protein was inhibited by ML-9, which suggested that mitogen-activated protein kinase may be one of the constituents in intracellular insuin signaling to the glucose transport system.
Natriuretic peptide receptors. We investigated the receptor selectivity of the natriuretic peptide family using the homologous assay system with endogeneous ligands, ANP, BNP and CNP, and recoptors, GC-A, GC-B and C-receptors, of the same species, which provided a new insight into the understanding of the physiological and clinical implications of the natriuretic peptide system. In intact aortic mcdia, GC-A recopptor was the major natriuretic peptide system. In intact aortic media, GC-A receptor was the major natriuretic peptide receptor. By contrast, in eultured
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aortic smooth muscle cclls expression of GC-B and C-receptors were inereased, which demonstrated that the maked phenotyperelated alteration occured in the expression of natriuretic peptide rcccptors in rat aortic smooth muscle cells
Endothelin receptors. We isolated the gene encoding the human endothejin-B receptor and determined its structural organization and ehromosomal asignment. The 5'-flanking region of the human endothelin-B receptor contained a sequence of potential Sp1 binding sites, some canonical consensus sequences of eis-elements including GATA motif, acute phase reactant regulatory element and E box. Using human-rodent somatic hybrid cell lines, the human endothelin-B recoptor gene was assigned to human chromosome 13.
Thyroid hormone receptor. We reported point mutations of the thyroid hormone beta1 gene in patients with generalized and pituitary resistance to thyroid hormone, which suggested that generalized and pituitary resistance to thyroid represent a continuous spectrum of the same etiological defect with variable tissue resistance to thyroid hormone. Less
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