2012 Fiscal Year Final Research Report
Mechanisms of COPII vesicle formation at ER exit sites
Project/Area Number |
22770121
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Single-year Grants |
Research Field |
Functional biochemistry
|
Research Institution | The University of Tokyo |
Principal Investigator |
|
Project Period (FY) |
2010 – 2012
|
Keywords | 小胞体 / 小胞輸送 / COPII 小胞 / ERES |
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.
|
Research Products
(6 results)