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Journal of Cellular Biochemistry

Retracted: Elevated expression of CaMKIIγ during osteoclastogenesis and its functional implications

Authors

  • Chaohua Yao,

    1. Department of Biomedical Sciences, College of Medicine at Rockford, UIC, Rockford, Illinois 61107
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  • Paula H. Stern,

    1. Department of Molecular Pharmacology & Biological Chemistry, Northwestern University, 303 E. Chicago Avenue, Chicago, Illinois 60611
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  • Liang Zhang

    Corresponding author
    1. Department of Biomedical Sciences, College of Medicine at Rockford, UIC, Rockford, Illinois 61107
    • Department of Biomedical Sciences, College of Medicine at Rockford, UIC, 1601 Parkview Avenue, Rockford, IL 61107.
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Abstract

Ca2+/calmodulin signaling has been recognized recently as a major regulator in osteoclastogenesis. Efforts have ensued to identify the downstream targets of this signaling pathway in the context of regulating osteoclastogenesis. The calcineurin-NFAT pathway has thus been identified as one such target. In this article, we describe the discovery of another novel downstream target, CaMKIIγ. We also demonstrate that CaMKIIγ is the sole known CaMK expressed in significant amounts in osteoclasts and their precursors. Other known CaMKs such as CaMKIV and CaMKIIα, β, δ, were not detectable, and CaMKI was only expressed at a negligible level. Furthermore, the expression of CaMKIIγ was tightly correlated with the osteoclastogenic process, with a peak level on Day 3 of cell culturing. Osteoclastogenesis is halted by treatment with the CaMKIIγ inhibitor, KN93, independently from apoptosis, with the IC50 for osteoclastogenesis matching that for blocking CaMKIIγ function. Collectively, these data indicate that CaMKIIγ may be a significant regulator of osteoclastogenesis. J. Cell. Biochem. 101: 1038–1045, 2007. © 2006 Wiley-Liss, Inc.

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