Truncation of parathyroid hormone in parathyroid cells
| Project/Area Number |
20590980
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Osaka City University |
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Principal Investigator |
INABA Masaaki Osaka City University, 大学院・医学研究科, 教授 (00176405)
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| Co-Investigator(Kenkyū-buntansha) |
IMANISHI Yasuo 大阪市立大学, 大学院・医学研究科, 講師 (50326253)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 人工透析学 / 副甲状腺アデノーマ / 2次性副甲状腺機能亢進症 / 副甲状腺ホルモン / カルシウム感知受容体 / N端断片化PT H / N端断片化PTH / 副甲状腺機能亢進症 |
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| Research Abstract |
Extracellular calcium concentration regulates parathyroid hormone (PTH) secretion via calcium-sensing receptor (CaR) on the parathyroid cell surface. N-terminal truncation of PTH is also regulated by extracellular calcium concentration. The N-terminal truncation is thought to be one of the regulatory mechanisms to secrete 1-84PTH from parathyroid cells, however, signal pathways of the mechanism in the cells are not yet reported. We attempt to determine whether the pathways of N-terminal truncation are identical from those of (1-84)PTH secretion in primary cultured human parathyroid cells. It is suggested that the N-terminal truncation of PTH regulated by extracellular calcium concentration has at least partly independent intracellular signaling systems from the (1-84)PTH secretion in human parathyroid cells.
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Report
(4 results)
Research Products
(86 results)
