ArticleWorld journal of orthopedics2012
Molecular mechanisms of triggering, amplifying and targeting RANK signaling in osteoclasts.
Article in World journal of orthopedics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
- Anti-osteoporotic effects of Yi Mai Jian on bone metabolism of ovariectomized rats.Frontiers in pharmacology · 2024Article
- Aster saponin AJournal of veterinary science · 2022Article
- Protective Effect of Ciclopirox against Ovariectomy-Induced Bone Loss in Mice by Suppressing Osteoclast Formation and Function.International journal of molecular sciences · 2021Article
- Sphingosylphosphorylcholine blocks ovariectomy-induced bone loss by suppressing CaJournal of cellular and molecular medicine · 2021Article
- RETRACTED: Fermented Sea Tangle (Foods (Basel, Switzerland) · 2019Article
- RETRACTED: Protective Effects of Fermented Oyster Extract against RANKL-Induced Osteoclastogenesis through Scavenging ROS Generation in RAW 264.7 Cells.International journal of molecular sciences · 2019Article
- Trans-pairing between osteoclasts and osteoblasts shapes the cranial base during development.Scientific reports · 2019Article
- The Role of Osteoprotegerin and Its Ligands in Vascular Function.International journal of molecular sciences · 2019Review
- Interleukin-27 prevents LPS-induced inflammatory osteolysis by inhibiting osteoclast formation and function.American journal of translational research · 2019Review
- mTORC1 impedes osteoclast differentiation via calcineurin and NFATc1.Communications biology · 2018Article
- Dectin-1 signaling inhibits osteoclastogenesis via IL-33-induced inhibition of NFATc1.Oncotarget · 2017Article
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- Conditional deletion of CD98hc inhibits osteoclast development.Biochemistry and biophysics reports · 2016Article
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- The Influence of DNA Methylation on Bone Cells.Current genomics · 2015Article
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- Vitamin D endocrine system and osteoclasts.BoneKEy reports · 2014Article
- RANKL-RANK interaction in immune regulatory systems.World journal of orthopedics · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoclast differentiation depends on receptor activator of nuclear factor-κB (RANK) signaling, which can be divided into triggering, amplifying and targeting phases based on how active the master regulator nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) is. The triggering phase is characterized by immediate-early RANK signaling induced by RANK ligand (RANKL) stimulation mediated by three adaptor proteins, tumor necrosis factor receptor-associated factor 6, Grb-2-associated binder-2 and phospholipase C (PLC)γ2, leading to activation of IκB kinase, mitogen-activated protein kinases and the transcription factors nuclear factor (NF)-κB and activator protein-1 (AP-1). Mice lacking NF-κB p50/p52 or the AP-1 subunit c-Fos (encoded by Fos) exhibit severe osteopetrosis due to a differentiation block in the osteoclast lineage. The amplification phase occurs about 24 h later in a RANKL-induced osteoclastogenic culture when Ca(2+) oscillation starts and the transcription factor NFATc1 is abundantly produced. In addition to Ca(2+) oscillation-dependent nuclear translocation and transcriptional auto-induction of NFATc1, a Ca(2+) oscillation-independent, osteoblast-dependent mechanism stabilizes NFATc1 protein in differentiating osteoclasts. Osteoclast precursors lacking PLCγ2, inositol-1,4,5-trisphosphate receptors, regulator of G-protein signaling 10, or NFATc1 show an impaired transition from the triggering to amplifying phases. The final targeting phase is mediated by activation of numerous NFATc1 target genes responsible for cell-cell fusion and regulation of bone-resorptive function. This review focuses on molecular mechanisms for each of the three phases of RANK signaling during osteoclast differentiation.
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