2007 Fiscal Year Final Research Report Summary
Development of a new therapy for diabetes mellitus through Betacellulin receptor cloning
| Project/Area Number |
17590915
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Metabolomics
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| Research Institution | Gunma University |
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Principal Investigator |
OKADA Shuichi Gunma University, Faculty of medicine, Medicine and Molecular Science, Assistant Professor (20260474)
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| Project Period (FY) |
2005 – 2007
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| Keywords | Regeneration / Betacelluli / EGF |
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| Research Abstract |
We tried to identify the Betacellulin receptor cloning. 1. We made two columns. The one contains Betacellulin (BTC/1-80) which is full length. The other one contains Betacellulin (BTG2-76) which is enough portion to evoke pancreatic beta cell differentiation. We focused on the molecule which not binds to BTC-1-80 column but binds to BTC/24-76 column. We could obtain EGF receptor and BTC seems to bind and use EGF receptor as well as EGF. We could not find any other candidate molecule containing receptor structure. 2. We speculated that there might be difference of phosphorylated molecule between BTC and EGF stimuli. We stimulated βHC9 cells with either BTC or EGF and tyrosine-phosphorylated molecules were pulled down by the design of immunoprecipitation with phosphotyrosine antibody. The separated band on SDS-PAGE, which is just unique for BTC stimulation, was isolated and processed LC/MS analysis. Finally we obtained a molecule containing phospholipase D active site motif with EGFR phosphorylation site. We considered that this molecule is regulating cell proliferation through Ras activation pathway of PLD2/SostRas. Further investigation is planned as a next step.
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