The analysis of the involvement of ER stress in FGFR3-related chondrodysplasias
Project/Area Number |
23791648
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Orthopaedic surgery
|
Research Institution | The University of Tokushima |
Principal Investigator |
|
Project Period (FY) |
2011 – 2012
|
Project Status |
Completed (Fiscal Year 2012)
|
Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
Keywords | 軟骨無形成症 / FGFR3 / 小胞体ストレス / 細胞死 |
Research Abstract |
Various point mutations of the Fibroblast Growth Factor Receptor(FGFR)3 Gene are known to cause short limb dwarfism. It is generally accepted that constitutive activation of the FGFR3 signaling is the main mechanism, but the severity of phenotype is not completely associated with the activation of FGFR3 signaling, suggesting the existence of the other mechanism. We showed the new mechanism that the accumulation of mutant FGFR3 in endoplasmic reticulum(ER) induced apoptosis of chondrocyte through ER stress.
|
Report
(3 results)
Research Products
(10 results)