2016 Fiscal Year Final Research Report
Study on molecular mechanism causing autoimmune retinopathy
| Project/Area Number |
25462723
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Ophthalmology
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2017-03-31
|
| Keywords | 網膜 / 自己免疫性網膜症 / リカバリン |
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| Outline of Final Research Achievements |
To elucidate the molecular pathology in autoimmune retinopathy (AIR), regulatory mechanism of expressions of autoantigen causing AIR as well as what kinds of role of such autoantigen aberrantly expressed in malignant tumor cells or none tumor cells were examined. Recoverin was identified to be expressed in 30-70% of cancer tissues. We observed co-precipitation of G-protein-coupled-kinases (GRKs) and caveolin-1 with Rec from cell lysates of 293 or SSTW cells. Immunocytechemistry revealed that immunoreactivities toward recoverin within the cancer cells were almost identical to those toward GRKs and caveolin-1. The present data strongly suggests that aberrantly expressed recoverin should be involved in the GRK-dependent cellular regulation in cancer cells.
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| Free Research Field |
眼科学
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