Mechanisms of small G protein Rac1 during limb development.
| Project/Area Number |
15K20557
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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 |
Surgical dentistry
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| Research Institution | Showa University |
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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 |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 細胞内シグナル伝達 / 細胞内シグナル / Rac1 |
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| Outline of Final Research Achievements |
Rac1 which is a member of the Rho small GTPases are known to be a regulator of multiple cellular functions, including cytoskeletal organization, proliferation, and apoptosis. Recently, its tissue-specific roles, especially in mammalian limb development, have been revealed using limb bud mesenchyme-specific inactivated Rac1 conditional knockout (Rac1 cKO) mice. In the present study, we employed in vitro micromass culture assays to define the underlying chondrogenic defect in Rac1 cKO mice. Micromass cultures derived from Rac1 cKO mice limbs lacked proliferation of chondrocytes compared to those from control mice limbs. These results suggested that Rac1 is required for proliferation of chondrocytes during limb development.
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Report
(4 results)
Research Products
(4 results)
