Explication of the cleft palate occurrence mechanism using p53 knock-out mouse
| Project/Area Number |
26861708
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Surgical dentistry
|
|---|
| Research Institution | Niigata University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2014-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | 口蓋口唇裂 / ｐ53 / 口蓋裂 / p53 / 口唇口蓋裂 / 放射線照射 |
|---|
| Outline of Final Research Achievements |
The purpose of this study was to investigate the role of p53 (a key regulator of apoptosis) in the pathogenesis of palatal cleft, with or without cleft lip. Palatal cleft is one of the most common congenital birth defects in humans. The palatal structure arises from five crucial developmental stages - initiation of palatal shelves; downgrowth of the palatal shelves; elevation of palatal shelves above the dorsal side of the tongue; horizontal growth of the palatal shelves; and fusion of paired palatal shelves at the midline. p53 was found to be expressed in the developing palatal shelves at all stages. The CL/Fr mouse strain is known to frequently exhibit spontaneous palatal cleft, with or without cleft lip. We found that the frequency of palatal cleft differed between CL/Fr mice with and without p53 mutation. Tissues displaying p53 expression were also consistent with the regions corresponding to palatal cleft and cleft lip.
|
Report
(3 results)
Research Products
(5 results)
