2011 Fiscal Year Final Research Report
Determine the novel amelogenin receptor which influence bone formation
| Project/Area Number |
21592605
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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 |
Orthodontic/Pediatric dentistry
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| Research Institution | Nagasaki University |
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Principal Investigator |
KONISHI Ikuri 長崎大学, 病院, 客員研究員 (00572380)
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| Co-Investigator(Kenkyū-buntansha) |
HOSHINO Tomonori 長崎大学, 病院, 講師 (00359960)
NISHIGUCHI Miyuki 長崎大学, 大学院医歯薬学総合研究科, 助教 (10253676)
HIDAKA Kiyoshi 長崎大学, 大学院医歯薬学総合研究科, 助教 (10389421)
FUJIWARA Taku 長崎大学, 大学院医歯薬学総合研究科, 助教 (00228975)
SATOU Kyouko 長崎大学, 病院, 助教 (70404499)
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| Project Period (FY) |
2009 – 2011
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| Keywords | アメロジェニン / 骨芽細胞 / 骨形成 / 受容体 |
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| Research Abstract |
Amelogenin stimulated about 23 kinds transcription factors in osteoblast. These transcription factors were analyzed by in silico data mining. This result was speculated that Amelogenin signaling pathways were ERK signal, Wnt/β-catenin signal and TGF-βBMP/ Smad signal. To confirm this result, it was inspected by a phosphorylation antibody whether Amelogenin through these signals in osteoblast or not.
Smad2/ 3/ 5 did not effect but ERK andβ-catenin were activated by amelogenin. Thus, it is suggested that novel amelogenin receptor not involving LAMP1 and CD63 may be Frizzled families which were a Wnt receptor.
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