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2017 Fiscal Year Final Research Report

Mechanisms of small G protein Rac1 during limb development.

Research Project

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Project/Area Number 15K20557
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Surgical dentistry
Research InstitutionShowa University

Principal Investigator

Saito Yoshiro  昭和大学, 歯学部, 助教 (70611581)

Project Period (FY) 2015-04-01 – 2018-03-31
Keywords細胞内シグナル伝達
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.

Free Research Field

骨代謝

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Published: 2019-03-29  

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