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In adult, bone is constantly removed by osteoclasts and replenished by osteoblasts. The coordinated action of osteoblasts and osteoclasts maintains the proper bone volume and calcium homeostasis. While Ca2+ MK-5108 is under the control of osteoblasts and osteoclasts, Ca2+ also regulates bone remodeling as an important intracellular second messenger. The increase of intracellular Ca2+ levels is considered to promote osteoblast proliferation and/or differentiation during bone remodeling [29] and [30]. Ca2+ signaling is mainly mediated by calmodulin (CaM) and calmodulin-dependent kinases (CaMKs) [18]. Several evidences strongly suggest that CaMKII plays an essential role in osteoblast differentiation [31]. The role of CaMKII in osteoblast differentiation is an interesting subject as Ca2+ signaling is also important for bone homeostasis. For this aspect, the regulation of Dlx5 function by CaMKII may play a significant role in osteoblast differentiation.
The activity of Dlx5 is regulated at the levels of transcription and post-translational modification. BMP-2 regulates the transcription of Dlx5 [14] and [32], while p38 regulates the transactivation activity of Dlx5 by phosphorylation [17]. Our results indicate that, during osteoblast differentiation, CaMKII regulates Dlx5 by phosphorylation.