Molecular analysis of craio-facial abnormalities found in the Sez12 knockout mice
Project/Area Number |
22592050
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Morphological basic dentistry
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Research Institution | Tokai University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
KIMURA Minoru 東海大学, 医学部, 教授 (10146706)
WATANABE Satoshi 独立行政法人農業生物資源研究所, ゲノム研究センター・家畜ゲノム, 主任研究員 (80391572)
|
Project Period (FY) |
2010 – 2012
|
Project Status |
Completed (Fiscal Year 2012)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | 22q11.2欠失症候群 / ノックアウトマウス / Sez12遺伝子 / 顎形態形成 / 22q11欠失症候群 / 軟骨内骨化 / Dgcr2 / Sez12 / Tbx1 / GFP / 関節軟骨 / 鼻中隔 / CT / Neural crest cell |
Research Abstract |
In this study, we investigated the relationship between the phenotype shown in the homozygous Sez12 knockout mice (Sez12-KO mice) and distribution of the knockin eGFP expression. We demonstrate that the Sez12 plays an important role in skeletal growth, such as cranial neural crest development during embryogenesis and endochondral ossification after birth. Furthermore, the Sez12 upregulation affected cell survival under a condition such as serum depletion. These findings suggest that the Sez12 is responsible for cell differentiation and maintenanceof the differentiating cells, which cause skeletal abnormalities in mice including craniofacial malformation.We analyzed the neuropathic pain and psychological outcome of patients following oral surgery.
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Report
(4 results)
Research Products
(44 results)