Pathophysiological significance of the splice variant of mouse TRPA1
| Project/Area Number |
25670290
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pain science
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| Research Institution | Okazaki Research Facilities, National Institutes of Natural Sciences |
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Principal Investigator |
Tominaga Makoto 大学共同利用機関法人自然科学研究機構(岡崎共通研究施設), 岡崎統合バイオサイエンスセンター, 教授 (90260041)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 疼痛学 / 生理学 / 神経科学 |
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| Outline of Final Research Achievements |
Transient receptor potential ankyrin 1 (TRPA1) is a nonselective cation channel. Although many studies suggest that TRPA1 is involved in inflammatory and neuropathic pain, its mechanism remains unclear. We identified an alternative splicing variant of the mouse Trpa1 gene. TRPA1a (full-length) and TRPA1b (splicing variant) physically interacted with each other, and TRPA1b increased the expression of TRPA1a in the plasma membrane. TRPA1a and TRPA1b co-expression significantly increased current density in response to different agonists. Exogenous overexpression of Trpa1b gene in wild-type DRG neurons also increased TRPA1a-mediated AITC responses. Moreover, expression levels of Trpa1a and Trpa1b mRNAs changed dynamically in two pain models (complete Freund’s adjuvant-induced inflammatory pain and partial sciatic nerve ligation-induced neuropathic pain models). These results suggest that TRPA1 may be regulated through alternative splicing under these pathological conditions.
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Report
(4 results)
Research Products
(12 results)
