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Publication : VapB as a regulator of osteoclastogenesis via modulation of PLCγ2-Ca(2+)-NFAT signaling.

First Author  Choi SW Year  2012
Journal  FEBS Lett Volume  586
Issue  3 Pages  263-9
PubMed ID  22245675 Mgi Jnum  J:179896
Mgi Id  MGI:5304594 Doi  10.1016/j.febslet.2011.12.033
Citation  Choi SW, et al. (2012) VapB as a regulator of osteoclastogenesis via modulation of PLCgamma2-Ca(2+)-NFAT signaling. FEBS Lett 586(3):263-9
abstractText  VapB has been shown to regulate calcium homeostasis in amyotrophic lateral sclerosis. Calcium signaling is also important in metabolic bone diseases, but the role of VapB in the generation of osteoclasts for bone resorption during osteoclastogenesis is not known. Therefore, we investigated the role of VapB in RANKL-induced osteoclast differentiation. Interestingly, VapB is induced during osteoclastogenesis, and regulates osteoclast differentiation by modulating NFATc1. The results also suggest that VapB regulates osteoclastogenesis via PLCgamma2-Ca(2+)-NFAT signaling. The involvement of PLCgamma2-Ca(2+)-NFAT signaling in VapB-regulated osteoclastogenesis was confirmed by a pharmacological study. Taken together, the results indicate that VapB positively regulates RANKL-mediated osteoclastogenesis via PLCgamma2-Ca(2+)-NFAT signaling.
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