Project/Area Number |
20591314
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Dermatology
|
Research Institution | Tohoku University |
Principal Investigator |
OKUYAMA Ryuhei Tohoku University, 医学部, 教授 (80292332)
|
Co-Investigator(Renkei-kenkyūsha) |
IKAWA Shuntaro 東北大学, 加齢医学研究所, 准教授 (50241576)
OGAWA EISAKU 信州大学, 医学部, 助授 (20451586)
|
Project Period (FY) |
2008 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2008: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | 表皮細胞 / p51 / p63 / シグナル伝達 / デスモプラキン / 乾癬 / p51/p63 / Desmoplakin / Perp / Bach |
Research Abstract |
p51/p63, a homologue of p53 tumor suppressor, is well known to play a role in oncogenesis. Simultaneously, p51/p63 promotes development of cellular characters specific for squamous cells, such as keratinocytes. Contrast to p51/p63, TGFβ suppresses these cellular characters as squamous cells, which leads to induction of cellular functions specific for mesenchymal cells. We focused on desmoplakin, calcium-dependent homophilic adhesion molecule, because the desmoplakin is a unique molecule in squamous cells. We found that desmoplakin expression is increased by p51/p63 whereas it is decreased by TGFβ.
|