PLCγ2 regulates osteoclastogenesis via its interaction with ITAM proteins and GAB2
J. Clin. Invest. Dailing Mao, et al. 116:2869 doi:10.1172/JCI28775 [
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Figure 5PLCγ2 modulates RANKL-mediated signaling. (
A) Activation of ERK and JNK in WT and
Plcg2–/– BMMs in response to M-CSF (100 ng/ml). PLCγ1 and PLCγ2 levels are shown. (
B) Western blot analysis of phospho-ERK, phospho-JNK, phospho–c-Jun, and phospho-IκBα in total cell lysates from WT and
Plcg2–/– BMMs stimulated with RANKL (100 ng/ml) for the indicated times. β-Actin blots served as loading control for
A and
B. (
C) Nuclear levels of phospho–c-Jun and p65 in nuclear extracts from WT and
Plcg2–/– BMMs stimulated with RANKL. (
D) The same samples used in
C were subjected to AP1 and NF-κB nonradioactive EMSA analysis. To control for binding specificity, a concentration of unlabeled oligonucleotides (U.O.) 200-fold greater than that recommended by the manufacturer was added to nuclear extracts from WT cells stimulated with RANKL for 60 minutes. SP1 served as loading control for
C and
D.
