ArticleProceedings of the National Academy of Sciences of the United States of America2008
RelB is the NF-kappaB subunit downstream of NIK responsible for osteoclast differentiation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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Who cites it
91 citing papers in PubMed, 144 citations in OpenAlex.
- Differential Effects of a First-in-Class IKKCalcified tissue international · 2026Article
- Uncovering functional INDELs responsible for splice sites in sheep with different immune profiles naturally exposed to gastrointestinal nematode infection.Scientific reports · 2025Article
- Characterization of a mouse model of osteoarticular infection using clinical isolates ofJBMR plus · 2025Article
- Single cell RNA-sequencing identified CCR7+/RELB+/IRF1+ T cell responding for juvenile idiopathic arthritis pathogenesis.Frontiers in immunology · 2025Article
- NF-κB in biology and targeted therapy: new insights and translational implications.Signal transduction and targeted therapy · 2024Review
- Nuclear Factor-Kappa B Regulation of Osteoclastogenesis and Osteoblastogenesis.Endocrinology and metabolism (Seoul, Korea) · 2023Article
- DNA-dependent protein kinase catalytic subunit binds to the transactivation domain 1 of NF-κB p65.Biochemistry and biophysics reports · 2023Article
- Mechanistic insight of interleukin-9 induced osteoclastogenesis.Immunology · 2023Article
- Toll-like receptor 4 signaling in osteoblasts is required for load-induced bone formation in mice.iScience · 2023Article
- New insights into the Lck-NF-κB signaling pathway.Frontiers in cell and developmental biology · 2023Review
- Dietary resistant starch alleviates Escherichia coli-induced bone loss in meat ducks by promoting short-chain fatty acid production and inhibiting Malt1/NF-κB inflammasome activation.Journal of animal science and biotechnology · 2022Article
- Article
- Conditional loss of IKKα in Osterix + cells has no effect on bone but leads to age-related loss of peripheral fat.Scientific reports · 2022Article
- Review
- IRF2 enhances RANKL-induced osteoclast differentiation via regulating NF-κB/NFATc1 signaling.BMB reports · 2021Article
- RelB and Neuroinflammation.Cells · 2021Review
- NullInternational journal of molecular sciences · 2021Article
- IKKe in osteoclast inhibits the progression of methylprednisolone-induced osteonecrosis.International journal of biological sciences · 2021Article
- Gamabufotalin Inhibits Osteoclastgenesis and Counteracts Estrogen-Deficient Bone Loss in Mice by Suppressing RANKL-Induced NF-κB and ERK/MAPK Pathways.Frontiers in pharmacology · 2021Article
- Identifying the Potential Differentially Expressed miRNAs and mRNAs in Osteonecrosis of the Femoral Head Based on Integrated Analysis.Clinical interventions in aging · 2021Article
31 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
NF-kappaB inducing kinase (NIK) is required for osteoclastogenesis in response to pathologic stimuli, and its loss leads to functional blockade of both alternative and classical NF-kappaB caused by cytoplasmic retention by p100. We now show that deletion of p100 restores the capacity of NIK-deficient osteoclast (OC) precursors to differentiate and normalizes RelB and p65 signaling. Differentiation of NIK-/- precursors is also restored by overexpression of RelB, but not p65. Additionally, RelB-/- precursors fail to form OCs in culture, and this defect is rescued by re-expression of RelB, but not by overexpression of p65. To further support the role of RelB in OCs, we challenged RelB-/- mice with TNF-alpha in vivo and found a diminished osteoclastogenic response. We then examined tumor-induced osteolysis in both RelB-/- and NIK-/- mice by using the B16 melanoma model. Growth of tumor cells in the bone marrow was similar to WT controls, but the absence of either RelB or NIK completely blocked the tumor-induced loss of trabecular bone. Thus, the alternative NF-kappaB pathway, culminating in activation of RelB, has a key and specific role in the differentiation of OCs that cannot be compensated for by p65.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.