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Since, Mundy G et al showed that statin, inhibitor of cholesterol (Ch) biosynthesis pathway, enhanced bone formation in rodents, the role of this pathway in hard tissues is actively observed. It is also known that Ch biosynthesis pathway produces some essential metabolites that are used as substrates for prenylation of small Gproteins such as Ras and Rho. We previously reported that Toxin B (Rho inhibitor) mimics the effects of statin on osteoblastic function and the dominant negative of Rac (N17Rac), one of Rho family proteins, stimulates osteoblastic bone formation in vitro. In this study, we tried to generate N17Rac transgenic mice (Tg) by the overexpression of N17Rac in osteoblast-specific manner and characterized the phenotype to examine the role of Rac in bone metabolism.

The Functional Involvement of Rac on Bone and Tooth Formation: Characteristic of N17Rac Transgenic Mice