| Project/Area Number |
24591366
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Endocrinology
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| Research Institution | Kochi University |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
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| Keywords | 副甲状腺ホルモン / カルシウム代謝 / 骨粗鬆症 / 副甲状腺 / カルシウム |
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| Outline of Final Research Achievements |
1.Parathyroid hormone (PTH) gene expression is inhibited by hypercalcemia, involving CaSR, NFAT, and Sp1/Sp6. 2. hypoparathyroidism, deafness, and renal dysplasia (HDR) syndrome is caused by GATA3 haploinsufficiency, and novel GATA3 mutation (R299Q) was identified. Decreased GATA3 activity causes decrease in GCM2 expression, with resultant defect in parathyroid development and PTH deficiency. 3. A variety of GCM2 gene mutation also causes congenital hypoparathyroidism.
Altogether, transcription factors GATA3, GCM2, and Sp1/Sp6 are supposed to be critical for the development and normal regulation of parathyroid gland, including PTH gene expression.
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