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. 2006 Oct 19;116(11):2869–2879. doi: 10.1172/JCI28775

Figure 8. TNF-α cannot correct the Plcg2–/– OC defect.

Figure 8

(A) WT and Plcg2–/– BMMs were stimulated with TNF-α (10 ng/ml) with time. Phosphorylated JNK, IκBα, and PLCγ2 were examined. β-Actin served as control. (B) WT and Plcg2–/– BMMs were cultured for 3 days with RANKL (100 ng/ml) and M-CSF (10 ng/ml). On day 3 TNF-α was also added to the culture media. Cells were fixed and TRAP stained at day 7. Magnification, ×200. (C) WT and Plcg2–/– preOCs were stimulated with TNF-α or RANKL for the indicated times, and expression levels of NFATc1, PLCγ2, and β-actin were determined.