| Project/Area Number |
24770098
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Structural biochemistry
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| Research Institution | Osaka University |
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Principal Investigator |
HASEGAWA Junya 大阪大学, 生命機能研究科, 助教 (00533788)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | イノシトールリン脂質 / エンドサイトーシス / SH3ドメイン / Multivesicular body / EGF |
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| Research Abstract |
The ubiquitinated signaling receptors such as the epidermal growth factor (EGF) receptor (EGFR) are delivered to early endosomes, and then sorted to lysosomes for degradation via multivesicular bodies (MVBs). The mechanism underlying the formation and scission of intraluminal vesicles to generate MVBs has remained elusive. In this study, we find that the localization of SH3YL1, which has been found by our group previously, shows the punctate pattern and the puncta is localized close to early endosomes. Deficiency of SH3YL1 prevents EGF trafficking from early to late endosomes, and inhibits the degradation of EGFR. Moreover, we show that loss of SH3YL1 results suppression of EGFR sorting into MVBs, indicating that SH3YL1 is required for the MVB biogenesis. Taken together, our observations reveal that an indispensable role of SH3YL1 in sorting of EGFR and MVB biogenesis.
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