Analysis of the molecular mechanism underlying ciliary function.
| Project/Area Number |
16K08583
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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 |
General medical chemistry
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| Research Institution | Osaka University |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 繊毛 / モデル動物 / 視細胞 / 網膜 / 内耳有毛細胞 / 脊椎動物モデル / IFT / 細胞・組織 / 神経科学 |
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| Outline of Final Research Achievements |
The cilia are organelles that project out from the cell surface in various types of cells. In humans, dysfunction of cilia causes a broad range of overlapping clinical phenotypes termed “ciliopathies,” which include retinal degeneration, polycystic kidney disease, polydactyly, and obesity. In certain ciliopathies, patients exhibit hyperphagia, obesity, and diabetes. Using the model animals including mice, zebrafish and goldfish, we analyzed molecular mechanisms underlining the function of cilia in vertebrates.
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| Academic Significance and Societal Importance of the Research Achievements |
ヒトにおいて繊毛機能の異常は、網膜色素変性症や、精神遅滞、摂食行動の異常による肥満・糖尿病、嚢胞腎、骨形成異常、不妊を含む「繊毛病」を引き起こすが、神経細胞において繊毛機能は特に重要であり、網膜における視細胞の繊毛異常は、網膜色素変性症などの視覚障害を伴う神経変性疾患を引き起こす。内耳有毛細胞の形成にも繊毛の機能が重要であることが明らかになりつつある。これらの疾患発症の分子メカニズムを明らかにすることで、疾患の予防や診断、治療法の確立に貢献することが期待される。
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Report
(4 results)
Research Products
(37 results)
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[Journal Article] miR-124 dosage regulates prefrontal cortex function by dopaminergic modulation.2019
Author(s)
Kozuka T, Omori Y, Watanabe S, Tarusawa E, Yamamoto H, Chaya T, Furuhashi M, Morita M, Sato T, Hirose S, Ohkawa Y, Yoshimura Y, Hikida T, Furukawa T.
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Journal Title
Sci Rep.
Volume: Mar 5;9(1)
Issue: 1
Pages: 3445-3445
DOI
NAID
Related Report
Peer Reviewed / Open Access
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[Journal Article] Loss of ift122, a Retrograde Intraflagellar Transport (IFT) Complex Component, Leads to Slow, Progressive Photoreceptor Degeneration Due to Inefficient Opsin Transport.2016
Author(s)
Boubakri M, Chaya T, Hirata H, Kajimura N, Kuwahara R, Ueno A, Malicki J, Furukawa T, Omori Y
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Journal Title
The Journal of Biological Chemistry
Volume: 291
Issue: 47
Pages: 24465-24474
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
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[Presentation] Retrograde IFT complex component defect causes slow, progressive photoreceptor degeneration due to inefficient opsin transport2016
Author(s)
Meriam Boubakri, Taro Chaya, Hiromi Hirata, Naoko Kajimura, Ryusuke Kuwahara, Akiko Ueno, Jarema Malicki, Takahisa Furukawa, Yoshihiro Omori,
Organizer
the 28th CDB Meeting
Place of Presentation
Riken CDB （兵庫県神戸市）
Related Report
Int'l Joint Research
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