Project/Area Number |
25462385
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Orthopaedic surgery
|
Research Institution | Jikei University School of Medicine |
Principal Investigator |
MAEDA KAZUHIRO 東京慈恵会医科大学, 医学部, 助教 (50548849)
|
Co-Investigator(Kenkyū-buntansha) |
齋藤 充 東京慈恵会医科大学, 医学部, 准教授 (50301528)
|
Project Period (FY) |
2013-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
|
Keywords | 破骨細胞 / 関節リウマチ / Wnt / Wnt |
Outline of Final Research Achievements |
I reported that Wnt5a enhances RANKL-induced osteoclastogenesis through noncanonical Wnt signaling which is the downstream of receptor tyrosine kinase Ror2, previously. Furthermore, we reported the possibility of the novel therapeutic target for rheumatoid arthritis by inhibiting it. In this study, we try to generate Ror2 inhibitor to inhibit Wnt noncanonical pathway. To try to generate the neutralizing antibody, we collected Ror2 protein using Ror2 overexpressing CHO cells, but failed. Because of this, we search for the low molecular compounds for inhibition of Wnt noncanonical pathway. As a result we found that the compound which inhibits some transcriptional factor suppressed wnt5a-enhanced osteoclastogenesis.
|