Analysis for the novel mechanisms of ectodermal dysplasia -the involvement of Store-operated calcium entry's abnormality-.
| Project/Area Number |
25893176
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Orthodontics/Pediatric dentistry
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| Research Institution | Kyushu University |
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Principal Investigator |
UMEDA Mariko 九州大学, 大学病院, その他 (40707618)
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| Project Period (FY) |
2013-08-30 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | STIM1 / 外胚葉異型性症 / ストア作動性カルシウム流入 / 遺伝子発現 / 外胚葉異形成症 |
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| Outline of Final Research Achievements |
The purpose of this study was to investigate the biological roles of store operated calcium entry (SOCE) regulated by STIM gene family, the possible novel responsible genes of ectodermal dysplasia, on epithelial cells/tissues.
Immunohistochemistry revealed that STIM1 protein was distinctively expressed in maturation stage of ameloblasts, and co-localized with the Claudin-1, a protein with important functions on epithelial cell-cell junctions. We established a method for fluoresce image analysis of intra-cellular calcium concentration in mouse incisors by using multi-photon microscopy. Furthermore, we performed phenotypic analysis of epithelial cell specific STIMs deficient mice, and found that the mice showed the phenotypes resembling human amelogenesis imperfecta.
These results suggest that the STIM1 plays important roles on enamel matrix mineralization through regulating the cellular SOCE and following functional changes.
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Report
(3 results)
Research Products
(2 results)
