The novel transcription factor Zfhx4 is critical to craniofacial development
| Project/Area Number |
15H06386
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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 |
Surgical dentistry
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| Research Institution | Osaka University |
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Principal Investigator |
NAKAMURA ERIKO 大阪大学, 歯学部附属病院, 特任助教(常勤) (00755069)
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| Project Period (FY) |
2015-08-28 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 転写因子 / 顎顔面骨格形成 / 口蓋裂 / 内軟骨性骨形成 / 口蓋 / 内軟骨整骨形成 |
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| Outline of Final Research Achievements |
Craniofacial development is regulated by several growth factors and cytokines, which regulate their down-stream transcription factors. Malfunction of these factors cause abnormal craniofacial disorders. A novel transcription factor Zfhx4 is putatively proposed to be responsible for the 8q21.11 Microdeletion Syndrome, characterized by a round face with full cheeks, ptosis, an underdeveloped alae, a short philtrum, micrognathia, low-set ears. To examine the role of Zfhx4 in craniofacial development, we first generated the Zfhx4-/- mice. Zfhx4-/- mice died of respiratory failure within a day after birth. Zfhx4-/- mice exhibited domed and short skull, micrognathia, malformation of coronoid process and cleft palate. Histological analyses indicated that tongue and tooth germ were normally formed in the E16.5 Zfhx4-/- mice. In situ hybridization analysis confirmed that Zfhc4 was expressed in Palatal shelf in vivo. Collectively, Zfhx4 plays a critical role in craniofacial development.
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Report
(3 results)
Research Products
(3 results)
