Study on the novel degradation pathway from recycling endosomes to lysosomes
| Project/Area Number |
24657125
|
|---|
| Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Cell biology
|
|---|
| Research Institution | Tohoku University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2012-04-01 – 2014-03-31
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
|---|
| Keywords | リサイクリングエンドソーム / リソソーム / 蛋白質分解 / トランスフェリン受容体 / アミノ酸トランスポーター / Rab / 低分子量G蛋白質 / 膜輸送 |
|---|
| Research Abstract |
Small GTPase Rab12 has recently been suggested to regulate a new membrane traffic pathway form recycling endosomes to lysosomes to degrade recycling molecules, but its physiological significance remained unknown. In this study, we found that Rab12 promotes constitutive degradation of PAT4 (proton-coupled amino-acid transporter 4). Because PAT4 is involved in the uptake of amino acids from the extracellular medium, knockdown of Rab12 in MEF cells increased the intracellular concentration of L-amino acids, resulting in the activation of mTORC1 and inhibition of autophagy. Our findings suggest that Rab12 suppresses excessive cell growth by maintaining the proper amount of PAT4 at the plasma membrane.
|
Report
(3 results)
Research Products
(19 results)
