| Project/Area Number |
26840036
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Functional biochemistry
|
|---|
| Research Institution | Osaka University |
|---|
Principal Investigator |
Misaki Ryo 大阪大学, 生物工学国際交流センター, 講師 (20571186)
|
|---|
| Project Period (FY) |
2014-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
|
|---|
| Keywords | Recycling endosome / Ras / Signal transduction / RasGRP / リサイクリングエンドソーム / シグナル伝達 / パルミトイル化 |
|---|
| Outline of Final Research Achievements |
In this study, it was suggested that a Ras-activation factor, RasGRP1, activates H-Ras localizing to recycling endosomes (REs). RasGRP1 colocalized with activated-Ras on REs but not with non-palmitoylated mutant Ras lacking the stable REs-localization. Inactivated RasGRP1 did not colocalize with Ras on REs strongly and the Ras was the inactivated form. Ras was also inactivated-form on REs under knockdown of endogenous RasGRP1 expression. Membrane of REs is known to have abundant phosphatidylserine (PS). However, establishment of PS synthase I-knockout cells resulted in no effect of PS depletion on the Ras-activation and the correct Ras localization. These results mean that activation of Ras on REs requires interaction with RasGRP1 and PS on REs does not affect function of RasGRP1.
|
