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Figure 9


Fig. 9. A diagram illustrating the role of JNK, CaMK and NFATc1 in maintaining the committed state during osteoclastogenesis by RANKL. JNK stimulates AP-1 transcription-factor activity and upregulates CaMKII and CaMKIV in committed pOCs. The elevated CaMK level in pOCs leads, through a mechanism yet to be elucidated, to a sustained increase in NFATc1 level, which is required to keep TRAP gene expression `on' in committed pOCs.





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