Nature Medicine
- 12, 1403 - 1409 (2006)
Published online: 26 November 2006; | doi:10.1038/nm1514
v-ATPase V0 subunit d2–deficient mice exhibit impaired osteoclast fusion and increased bone formationSeoung-Hoon Lee, Jaerang Rho, Daewon Jeong, Jai-Yoon Sul, Taesoo Kim, Nacksung Kim, Ju-Seob Kang, Takeshi Miyamoto, Toshio Suda, Sun-Kyeong Lee, Robert J Pignolo, Boguslawa Koczon-Jaremko, Joseph Lorenzo & Yongwon Choi Supplementary Fig. 1 (pdf 256K)
Supplementary Figure 1 (a) Mouse and human Atp6v0d2 amino acid sequences, identified in this study, are shown. Supplementary Fig. 2 (pdf 308K)
(a-b) Deficiency of Atp6v0d2 does not affect function of the kidney. Supplementary Fig. 3 (pdf 236K)
(a-b) Deficiency of Atp6v0d2 does not affect v-ATPase activity of osteoclasts. Supplementary Fig. 4 (pdf 124K)
Real-time PCR of RNA from wild-type (WT) and Atp6v0d2-/- osteoclasts. Supplementary Fig. 5 (pdf 112K)
Real-time PCR of ADAM family genes from wild-type (WT) and Atp6v0d2-/-osteoclasts. T Supplementary Fig. 6 (pdf 184K)
(a) DC-STAMP-deficient cells express Atp6v0d2 mRNA and protein at levels similar to wild-type cells. Supplementary Fig. 7 (pdf 200K)
(a) RANK expression or its signaling is not affected in the absence of Atp6v0d2. Supplementary Table 1 (pdf 276K)
(a) Structural Parameters measured by Microcomputed Tomography (b) Static histomorphometric parameters of bone structure in femur of wild-type (WT) and Atp6v0d2-/- (KO) mice. Supplementary Methods (pdf 56K)
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