| Project/Area Number |
20770112
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Functional biochemistry
|
|---|
| Research Institution | Tokyo Metropolitan Organization for Medical Research |
|---|
Principal Investigator |
MATSUDA Noriyuki Tokyo Metropolitan Organization for Medical Research, 東京都臨床医学総合研究所, 主任研究員 (10332272)
|
|---|
| Project Period (FY) |
2008 – 2009
|
| Project Status |
Completed (Fiscal Year 2009)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
|
|---|
| Keywords | ユビキチン / パーキンソン病 / Parkin / PINK1 / 細胞膜修復 / MG53 / RING finger motif |
|---|
| Research Abstract |
Parkinson's disease (PD) is a prevalent neurodegenerative disorder. Recent identification of genes linked to familial forms of PD, such as Parkin and PINK1, has revealed that ubiquitylation and mitochondrial integrity are key factors in disease pathogenesis. However, the exact mechanism underlying the functional interplay between Parkin-catalyzed ubiquitylation and PINK1-regulated mitochondrial quality control remains an enigma. We revealed the concrete mechanism underlying the functional interplay between ubiquitylation catalyzed by Parkin and mitochondrial quality control regulated by PINK1. These results provide crucial insight into the pathogenic mechanisms of PD. We also revealed that MG53 ubiquitin ligase is involved in plasma-membrane repair.
|
