Studies on the coupling mechanism between lysobisphosphatidic acid (LBPA) and S1P signaling
| Project/Area Number |
15K15066
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
General medical chemistry
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| Research Institution | Kobe University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
OKADA Taro 神戸大学, 大学院医学研究科, 准教授 (80304088)
KAJIMOTO Taketoshi 神戸大学, 大学院医学研究科, 助教 (00509953)
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| Project Period (FY) |
2015-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
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| Keywords | スフィンゴシン１リン酸 / S1P / エンドソーム / エキソソーム / リゾビスフォスファチジン酸 / LBPA / スフィンゴシンキナーゼ / 後期エンドソーム |
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| Outline of Final Research Achievements |
We have studied the mechanism underlying how sphingosine kinase 2 (SphK2), which plays a key role to regulate the maturation of exosomal multivesicular endosomes (exosomal MVEs), is recruited to exosomal MVEs. We focused on a specific marker lipid for MVEs, lysobisphosphatidic acid (LBPA) for the recruitment of SphK2 to MVEs. We found a strong binding of SphK2 to this lipid as assessed by a dot-blot overlay assay. Next, immunocytochemistry of COS7 cells expressing both SphK2-GFP and CD63-mCherry with anti-LBPA antibody showed that there existed LBPA-positive MVEs, which were devoid of SphK2. Further studies are necessary to clarify the causal relationship between the two molecules.
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Report
(2 results)
Research Products
(3 results)
