2012 Fiscal Year Final Research Report
Mechanisms of COPII vesicle formation at ER exit sites
| Project/Area Number |
22770121
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Functional biochemistry
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2010 – 2012
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| Keywords | 小胞体 / 小胞輸送 / COPII 小胞 / ERES |
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| Research Abstract |
COPII vesicles are formed at the ER exit sites, which mediate the ER-to-Golgi traffic. Sec16 acts as a key factor for ERES formation as well as COPII-mediated transport. Here we have shown that Sec16 is self-assembled to form a homooligomer on the membranes. In addition, we find that Sec16 negatively regulates activation of Sar1 GTP hydrolysis by COPII coat proteins.
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