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NF-κB-Mediated Regulation of Osteoclastogenesis

Boyce, Brendan F., Xiu, Yan, Li, Jinbo, Xing, Lianping, Yao, Zhenqiang·2015·Endocrinology and Metabolism
DOI 10.3803/enm.2015.30.1.35PMC PMC4384681
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Fig. 1 Canonical and non-canonical nuclear factor-kappa B (NF-κB) signaling induced by receptor activator of NF-κB ligand (RANKL) and tumor necrosis factor (TNF). RANKL and TNF induce canonical signaling by recruiting TNF receptor (TNFR)-associated factor 6 (TRAF6) and TRAF2/5, respectively, to their receptors to activate a complex consisting of IκB kinase (IKK)-α, IKK-β and IKK-γ (NF-κB essential modulator, NEMO), which induces phosphorylation and degradation of IκB-α and the release of p65/p50 heterodimers, which translocate to the nucleus. This induces expression of c-Fos and nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1), two other transcription factors necessary for osteoclast precursor differentiation, as well as the inhibitory κB protein, NF-κB p100. In un-stimulated cells, p100 binds to RelB to prevent its translocation to the nucleus. RANKL induces the ubiquitination and lysosomal degradation of TRAF3 through TRAF2/cellular inhibitor of apoptosis 1/2 (cIAP1/2), releasing NF-κB-inducing kinase (NIK) to activate (phosphorylate) IKK-α, which leads to proteasomal processing of p100 to p52; RelB:p52 heterodimers then go to the nucleus to induce target gene expression. TNF does not degrade TRAF3, and thus NIK is degraded, leading to the accumulation of p100 in the cytoplasm of osteoclast precursors to limit their differentiation [3,4].
Fig. 1 Canonical and non-canonical nuclear factor-kappa B (NF-κB) signaling induced by receptor activator of NF-κB ligand (RANKL) and tumor necrosis factor (TNF). RANKL and TNF induce canonical signaling by recruiting TNF receptor (TNFR)-associated factor 6 (TRAF6) and TRAF2/5, respectively, to their receptors to activate a complex consisting of IκB kinase (IKK)-α, IKK-β and IKK-γ (NF-κB essential modulator, NEMO), which induces phosphorylation and degradation of IκB-α and the release of p65/p50 heterodimers, which translocate to the nucleus. This induces expression of c-Fos and nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1), two other transcription factors necessary for osteoclast precursor differentiation, as well as the inhibitory κB protein, NF-κB p100. In un-stimulated cells, p100 binds to RelB to prevent its translocation to the nucleus. RANKL induces the ubiquitination and lysosomal degradation of TRAF3 through TRAF2/cellular inhibitor of apoptosis 1/2 (cIAP1/2), releasing NF-κB-inducing kinase (NIK) to activate (phosphorylate) IKK-α, which leads to proteasomal processing of p100 to p52; RelB:p52 heterodimers then go to the nucleus to induce target gene expression. TNF does not degrade TRAF3, and thus NIK is degraded, leading to the accumulation of p100 in the cytoplasm of osteoclast precursors to limit their differentiation [3,4].CC BY-NC · PubMed Central

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Cited by

Metadata

Authors
Boyce, B. F., Xiu, Y., Li, J., Xing, L., & Yao, Z.
Affiliations
Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, USA.
Venue
Endocrinology and Metabolism
Publisher
Korean Endocrine Society
Published
2015
Volume
30
Issue
1
Pages
35
ISSN
  • 2093-596X
  • 2093-5978
DOI
10.3803/enm.2015.30.1.35
PMC
PMC4384681
Cited by
299
References
7
Language
en
Licence
creativecommons.org/licenses/by-nc/3.0/ (tdm)
Funders
National Institute of Health PHS (AR043510, AR48697, AR63650)

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