Fig. 6: Nf2-FAK interaction mediated PI3K/AKT and ERK1/2 signaling in osteoblasts. | Nature Communications

Fig. 6: Nf2-FAK interaction mediated PI3K/AKT and ERK1/2 signaling in osteoblasts.

From: Nf2-FAK signaling axis is critical for cranial bone ossification and regeneration

Fig. 6

a The activities of phospho-PLC-γ and phospho-Akt were particularly reduced in Nf2 mutant osteoblasts. b The activity of phospho-Erk1/2 was specially decreased, and while the activities of phospho-p38 and phospho-JNK were not altered in Nf2 mutant osteoblasts (ab). ce In Nf2 mutant primary osteoblasts, coIP assay showed that Nf2 deletion led to decreased connection between FAK and PI3K catalytic subunit p110. f, g The immunosignals of phospho-Akt and phospho-Erk1/2 at sagittal section of E18.5 skull tissue were notably reduced in Nf2 mutants (arrow). h, i The immunosignals of phospho-Akt and phospho-Erk1/2 in Nf2 mutants at the section of E12.5 cranial primordium were remarkably decreased in Runx2+ osteoprogenitors (arrow). Scale bar: 50 μm in (h), 100 μm in (f, i). Data were expressed as means ± SD and each dot represents an individual biological replicate. P values were calculated by unpaired Student’s t-test with two-tailed analysis without adjustments. OB, primary osteoblasts.

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