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. 2006 Nov 1;20(21):2937–2942. doi: 10.1101/gad.1482906

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Copyright © 2006, Cold Spring Harbor Laboratory Press

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Figure 3. — Runx2 regulates chondrocyte proliferation through Fgf18. (A) In situ hybridization analysis of Fgf18 expression in ribs and humeri of E15.5 wild-type (WT), α1(I) Twist-1, Runx2 ^+/−, CC/CC, and ΔTwist box ^−/− embryos. Perichondrial Fgf18 expression is decreased in α1(I) Twist1 and Runx2 ^+/− and increased in CC/CC and ΔTwist box ^−/− embryos. (B) BrdU incorporation analysis in ribs and humeri at E14.5 and E16.5 of wild-type, Fgf18 ^+/−, Runx2 ^+/−, Fgf18 ^+/− ; Runx2 ^+/−, and Fgf18 ^−/− embryos. Chondrocyte proliferation is similarly increased in Fgf18 ^+/− ; Runx2 ^+/− and Fgf18 ^−/− embryos. (C) Histological and in situ hybridization analysis of α1(X) Collagen and Osteocalcin expression in humeri of E16.5 wild-type, Fgf18 ^+/−, Runx2 ^+/−, Fgf18 ^+/− ; Runx2 ^+/−, and Fgf18 ^−/− embryos. (D) Real-time PCR analysis of α1 Integrin expression in humeri of E15.5 wild-type, Runx2 ^+/−, Fgf18 ^+/−, Fgf18 ^−/−, and Runx2 ^+/− ; Fgf18 ^+/− embryos, normalized to β-actin.