Fig. 7: Activation of FAK mediated ERK and AKT signaling rescued the deficiency in Nf2 mutant osteoblasts.

a The inhibition of the FAK activity using inhibitor PF573228 resulted in significantly decreased activities of phospho-Erk1/2 and phospho-Akt and reduced activities of Runx2 and Sp7 in primary osteoblasts for 24 h. b The pharmaceutical activation of FAK on phospho-FAK (397) using Adhesamine (50 μM) can sufficiently rescue the activities of phospho-397FAK and its downstream signaling phospho-Erk1/2 and phospho-Akt in Nf2 mutant osteoblasts for 24 h. c Adding Akt activator, Erk1/2 activator, and FAK activator in primary osteoblasts for 14 days can sufficiently rescue deficient ossification in Nf2 mutant osteoblasts, and solvents used for the activators applied to the control groups. Data were expressed as means ± SD with at least three biological replicates. Scale bar: 50 μm in (c). OB, primary osteoblasts.