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Fig. 7. Role of CaMK in the JNK-dependent maintenance of the committed state. (A) Relative signal intensity of CaMKIV from the DNA microarray analysis of three different human samples (1-3) described in the Materials and Methods is presented. (B) Mouse BMM-derived pOCs were treated with (+SP) or without (–SP) SP600125 (10 µM) for 24 hours in the presence of RANKL (100 ng/ml) and M-CSF (30 ng/ml). Expression of CaMKII
, CaMKII
and CaMKIV was examined by real-time PCR. (C-E) pOCs were transfected with oligonucleotides for CamKII and/or CamKIV siRNA. (C) Knockdown of CaMK expression was confirmed by reverse transcriptase (RT)-PCR. (D) Cells were TRAP-stained and the percentage of TRAP+ cells was determined. (E) Cells were also evaluated for phagocytic activity with FITC-labeled zymosan. (B,D,E) Error bars represent s.d. from triplicate samples. Results are representative of three independent experiments.
