Analysis of molecular mechanism of tumor progression induced by an alpha6beta4 integrin
Project/Area Number |
23790373
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Pathological medical chemistry
|
Research Institution | Fukushima Medical University |
Principal Investigator |
|
Project Period (FY) |
2011 – 2012
|
Project Status |
Completed (Fiscal Year 2012)
|
Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
Keywords | β4インテグリン / 癌 / 糖鎖 / β4インテグリン / インテグリン |
Research Abstract |
In this study, to elucidate the role of N-glycosylation on β4 integrin, we established the keratinocytes re-expressing wild-type or N-glycosylation-defective β4 integrin in β4 integrin null keratinocytes. The analysis using the keratinocytes indicated that N-glycosylation plays important roles for integrin-mediated cell adhesion and migration. In addition, we found that β4 integrin forms supramolecular complex with EGFR through cross-linking with galectin-3-mediated N-glycans, thereby promoting cellular signaling and the following cellular function.
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Report
(3 results)
Research Products
(12 results)