1995 Fiscal Year Final Research Report Summary
Study on the soluble form TSH receptor
| Project/Area Number |
05670836
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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 | Gunma University |
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Principal Investigator |
MURAKAMI Masami Gunma University, 医学部・第一内科, 助手 (30241871)
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| Project Period (FY) |
1993 – 1995
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| Keywords | TSH receptor / Graves' disease / Molecular biology / Thyroid / Soluble form receptor |
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| Research Abstract |
Using rabbit antisera against a peptide corresponding to the N-terminus of the TSH receptor, we identified TSH receptor-like immunoreactivity in human peripheral blood, which may contribute to the pathogenesis of Graves' disease. This immunoreactivity may result from the secretion of truncated form of the TSH receptor lacking transmembrane domain. Northern blot analysis of human thyroid tissue identified 1.7kb and 1.3kb variants of TSH receptor, other than full length form that is 4.3kb. We cloned 1.3kb variant of TSH receptor, which is identical to the one reprted by Graves et al. We produced antisera against the unique amino acid sequence at the C-terminus of the variant and established the RIA system. However, we were not able to detect the immunoreactivity of this variant in human peripheral blood nor in the medium of CHO cells expressing this 1.3kb variant. Although we have attempted cloning of 1.7kb variant using thyroid cDNA library, Hunt et al. have just reported the molecular cloning of 1.7kb variant. Confirmation of the 1.7kb variant is in progress in our laboratory. We are also trying to purify TSH receptor-like immunoreactivity in human peripheral blood using purified TSH receptor related peptide antisera.
During the period of this research, we reported the clinical usefulness of TSAb measurement using CHO-cells expressing human TSH receptors for the diagnosis and follow up of Graves' disease. We also reported that the antisera against the peptide of N-terminus of extracellular domain of TSH receptor stimulated and the antisera against the peptide of C-terminus inhibited CHO cells expressing human TSH receptors.
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