Analysis of PLCipsiron-PKCmicro passway in psoriasis, dermatitis ,carcinogenesis, and cataract
| Project/Area Number |
15K19689
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Dermatology
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| Research Institution | Tohoku Medical and Pharmaceutical University (2016-2017)
Kobe University (2015) |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | PLCε / プロテインキナーゼC / 皮膚炎症 / 乾癬 / ホスホリパーゼCε / 皮膚発癌 / 紫外線 / 白内障 |
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| Outline of Final Research Achievements |
We have found K5 - PLCε - transgenic (TG) mouse to express specifically at skin keratinocytes had scales, acanthosis, parakeratosis, infiltration of neutrophils at epidermis. These clinical and histological changes was concordant with psoriasis vulgaris. We confirmed PLCε activated PKCμ in vitro, and then we have created a transgenic mouse (K5 - PKCμ- TG mouse) to express specifically at skin keratinocytes.
their skin didn’t have the characteristics at like psoriasis vulgaris.
From the above, the overexpression of PLCε at keratinocytes cause the change like psoriasis without PKCμ activation.
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Report
(4 results)
Research Products
(15 results)
