Novel osteoclast signaling mechanisms.
作者： Masahiro Shinohara , Hiroshi Takayanagi
DOI: 10.1007/S11914-007-0005-1
关键词: Calcium signaling 、 Receptor 、 Immunoreceptor tyrosine-based activation motif 、 NFAT 、 NFATC Transcription Factors 、 Cancer research 、 Chemistry 、 Osteoclast 、 Transcription factor 、 RANKL
摘要: Osteoclasts are cells of monocyte/macrophage origin that degrade bone matrix. Receptor activator NF-κB ligand (RANKL) induces osteoclast differentiation in the presence macrophage colony-stimulating factor. RANKL activates tumor necrosis factor receptor-associated 6, c-Fos, and calcium signaling pathways, all which indispensable for induction activation nuclear activated T (NFAT) c1. NFATc1 is master transcription differentiation, regulates many osteoclast-specific genes. Multiple immunoglobulin-like receptors associated with immunoreceptor tyrosine-based motif (ITAM)-harboring adapters, Fc receptor common γ subunit (FcRγ), DNAX-activating protein (DAP) 12 mediate costimulatory signals RANK, activate through phospholipase Cγ (PLCγ). In addition to calcineurin-NFATc1, CaMK-CREB (calcium/calmodulin kinase-cyclic AMP-response element binding protein) pathway, also plays a critical role osteoclastogenesis. This review summarizes recent advances study mechanisms differentiation.
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