Binding a bent integrin

FGF gets in your bones nt-mediated differentiation of bone precursors gets shut down, say Mansukhani et al. on page 1065, if there is too much FGF receptor (FGFR) activity. Bones form through the maturation of osteoblasts. This process is disrupted in the skulls of patients with activating mutations in FGFR1 and FGFR2. The new evidence suggests that FGF counteracts differentiation by blocking Wnt. Microarray analysis revealed that, although Wnt-regulated genes are normally turned on in maturing osteoblasts, their activation is dampened in the overactive FGFR mutant osteoblasts. A major mediator of the FGF-induced Wnt down-regulation seems to be the Sox2 transcription factor. Normally associated with neurons or embryonic stem cells, Sox2 is now shown to be strongly expressed in osteoblasts when FGF signaling is high. Sox2 was associated with -catenin in osteoblasts and blocked Wnt W