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- W1995269092 abstract "Osteoclasts are responsible for bone resorption and play a pivotal role in the pathogenesis of osteolytic disorders. NF-kappaB is a set of nuclear factors that bind to consensus DNA sequences called kappaB sites, and is essential for osteoclast formation and survival. NF-kappaB signalling pathways are strictly regulated to maintain bone homeostasis by cytokines such as RANKL, TNF-alpha and IL-1, which differentially regulate classical and/or alternative NF-kappaB pathways in osteoclastic cells. These pathways are also modulated by NF-kappaB mediators, including TRAF6, aPKC, p62/SQSTM1 and deubiquitinating enzyme CYLD that are involved in the ubiquitin-proteasome system during RANK-mediated osteoclastogenesis. Abnormal activation of NF-kappaB signalling in osteoclasts has been associated with excessive osteoclastic activity, and frequently observed in osteolytic conditions, including periprosthetic osteolysis, arthritis, Paget's disease of bone, and periodontitis. NF-kappaB modulators such as parthenolide and NEMO-binding domain peptide demonstrate therapeutic effects on inflammation-induced bone destruction in mouse models. Unravelling the structure and function of NF-kappaB pathways in osteoclasts and other cell types will be important in developing new strategies for treatments of bone diseases." @default.
- W1995269092 created "2016-06-24" @default.
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- W1995269092 date "2009-02-01" @default.
- W1995269092 modified "2023-10-16" @default.
- W1995269092 title "NF-κB modulators in osteolytic bone diseases" @default.
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- W1995269092 doi "https://doi.org/10.1016/j.cytogfr.2008.11.007" @default.
- W1995269092 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19046922" @default.
- W1995269092 hasPublicationYear "2009" @default.
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