ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2007
RGS12 is essential for RANKL-evoked signaling for terminal differentiation of osteoclasts in vitro.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 64 citations in OpenAlex.
- Cell signaling and transcriptional regulation of osteoclast lineage commitment, differentiation, bone resorption and diseases.Cell discovery · 2026Review
- The role of RGS12 in tissue repair and human diseases.Genes & diseases · 2025Review
- RGS1 Enhancer RNA Promotes Gene Transcription by Recruiting Transcription Factor FOXJ3 and Facilitates Osteoclastogenesis Through PLC-IP3R-dependent CaInflammation · 2025Article
- Nano-Based Drug Delivery Systems for Periodontal Tissue Regeneration.Pharmaceutics · 2022Review
- IFT80 negatively regulates osteoclast differentiation via association with Cbl-b to disrupt TRAF6 stabilization and activation.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- RGS12 Drives Macrophage Activation and Osteoclastogenesis in Periodontitis.Journal of dental research · 2022Article
- Effect of Regulator of G Protein Signaling Proteins on Bone.Frontiers in endocrinology · 2022Review
- Metabolic acidosis regulates RGS16 and G protein signaling in osteoblasts.American journal of physiology. Renal physiology · 2021Article
- RGS12 is a novel tumor suppressor in osteosarcoma that inhibits YAP-TEAD1-Ezrin signaling.Oncogene · 2021Article
- Finely-Tuned Calcium Oscillations in Osteoclast Differentiation and Bone Resorption.International journal of molecular sciences · 2020Review
- Regulator of G protein signaling 10: Structure, expression and functions in cellular physiology and diseases.Cellular signalling · 2020Review
- The co-culture of ASCs and EPCs promotes vascularized bone regeneration in critical-sized bone defects of cranial bone in rats.Stem cell research & therapy · 2020Article
- Article
- Regulator of G Protein Signaling Protein 12 (Rgs12) Controls Mouse Osteoblast Differentiation via Calcium Channel/Oscillation and Gαi-ERK Signaling.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019Article
- A role for Regulator of G protein Signaling-12 (RGS12) in the balance between myoblast proliferation and differentiation.PloS one · 2019Article
- Comparative Characterization of Osteoclasts Derived From Murine Bone Marrow Macrophages and RAW 264.7 Cells Using Quantitative Proteomics.JBMR plus · 2018Article
- Genetic Analysis of Rare Human Variants of Regulators of G Protein Signaling Proteins and Their Role in Human Physiology and Disease.Pharmacological reviews · 2018Review
- Expression regulation and functional analysis of RGS2 and RGS4 in adipogenic and osteogenic differentiation of human mesenchymal stem cells.Biological research · 2017Article
- Regulators of G protein signaling 12 promotes osteoclastogenesis in bone remodeling and pathological bone loss.Cell death and differentiation · 2015Article
- Activators of G protein signaling in the kidney.The Journal of pharmacology and experimental therapeutics · 2015Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledHow RANKL evokes [Ca(2+)](i) oscillations and leads to osteoclast differentiation is unclear. We identified a new signaling protein, RGS12, and found that RGS12 is essential for [Ca(2+)](i) oscillations and osteoclast differentiation induced by RANKL. RGS12 may play a critical role in the RANKL-evoked PLCgamma-calcium channels-[Ca(2+)](i) oscillation-NFAT2 pathway.
introductionRANKL-induced [Ca(2+)](i) oscillations play a switch-on role in NFAT2 expression and osteoclast differentiation. However, RANKL evokes [Ca(2+)](i) oscillations and leads to osteoclast differentiation by an unknown mechanism. In this study, we identified a new RANKL-induced signaling protein, regulator of G signaling protein 12 (RGS12), and investigated its effect on osteoclast differentiation in vitro. MATERIALS AND
methodsWe used a genome-wide screening approach to identify genes that are specifically or prominently expressed in osteoclasts. To study the role of the RGS12 in osteoclast differentiation, we used vector and lentivirus-based RNAi gene silencing technology to silence the RGS12 gene in the monocyte progenitor cell lines and primary bone marrow-derived monocytes (BMMs). The interaction between RGS12 and N-type calcium channels was elucidated using co-immunoprecipitation and immunoblotting.
resultsWe found that RGS12 was prominently expressed in osteoclast-like cells (OLCs) induced by RANKL. This result was further confirmed at both the mRNA and protein level in human osteoclasts and mouse OLCs. Silence of RGS12 expression using vector and lentivirus based RNA interference (RNAi) impaired phosphorylation of phospholipase C (PLC)gamma and blocked [Ca(2+)](i) oscillations, NFAT2 expression, and osteoclast differentiation in RANKL-induced RAW264.7 cells and BMMs. We further found that N-type calcium channels were expressed in OLCs after RANKL stimulation and that RGS12 directly interacted with the N-type calcium channels.
conclusionsThese results reveal that RGS12 is essential for the terminal differentiation of osteoclasts induced by RANKL. It is possible that RGS12 regulates osteoclast differentiation through a PLC gamma-calcium channel-[Ca(2+)](i) oscillation-NFAT2 pathway.
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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.