Affinage

TNFRSF11B

Tumor necrosis factor receptor superfamily member 11B · UniProt O00300

Length
401 aa
Mass
46.0 kDa
Annotated
2026-06-10
46 papers in source corpus 16 papers cited in narrative 16 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/6 claims corpus-supported (83%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TNFRSF11B encodes osteoprotegerin (OPG), a secreted decoy receptor that restrains osteoclast differentiation and bone resorption by sequestering RANKL, with its activity depending on an N-terminal cysteine-rich ligand-binding domain and C-terminal cysteine-mediated homodimerization (PMID:12189164, PMID:15777670). Loss-of-function mutations operate through two convergent mechanisms: missense changes in the cysteine-rich domain disrupt RANKL binding with severity scaling to the degree of binding loss, while truncating/frameshift mutations remove the C-terminal cysteine, abolish homodimerization, and reduce RANKL-binding capacity, releasing osteoclastogenesis from inhibition (PMID:14672344, PMID:15777670, PMID:17352649). A knock-in murine model recapitulates this, producing osteopenia, elevated bone remodeling, increased osteoclast activity, and CPPD-associated joint pathology (PMID:41826214). A read-through allele (OPG-XL), once classified as gain-of-function, behaves as loss-of-function for RANKL-mediated osteoclastogenesis with reduced binding to osteoblastic cells (PMID:24743232, PMID:33559312). OPG expression is controlled at multiple levels — by functional promoter and splicing polymorphisms (PMID:21994215), by circadian clock genes Bmal1 and REV-ERBα downstream of α1B-adrenergic signaling in osteoblasts (PMID:26453621), and by miR-145 in chondrocytes (PMID:27922673). Beyond the skeletal RANKL axis, OPG drives a chondrocyte-to-osteoblast transition in articular cartilage independently of RANK/RANKL (PMID:33989379), and in tumors it activates Wnt/β-catenin signaling via direct binding and phosphorylation of GSK-3β in gastric cancer (PMID:32398963) and the PI3K/AKT pathway in bladder cancer (PMID:39481664).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2002 High

    Established that disease-associated TNFRSF11B mutations act by abolishing OPG's functional ability to suppress bone resorption, defining the gene's loss-of-function mechanism.

    Evidence Recombinant wild-type vs. mutant OPG from HEK conditioned medium in an in vitro bone resorption assay

    PMID:12189164

    Open questions at the time
    • Did not resolve whether the defect was in RANKL binding, dimerization, or secretion
    • Single mutation tested
  2. 2003 Medium

    Resolved a genotype-phenotype correlation by linking mutation location within the cysteine-rich ligand-binding domain to severity of RANKL-binding disruption.

    Evidence Mutation analysis across affected families with structural prediction correlated to clinical severity

    PMID:14672344

    Open questions at the time
    • Functional effects predicted, not directly measured by binding assay
    • No structural model verified
  3. 2005 High

    Demonstrated that C-terminal truncation abolishes OPG homodimerization and reduces RANKL binding, mechanistically tying dimerization to full activity.

    Evidence Transient overexpression with Western blot for dimerization and ELISA for RANKL binding

    PMID:15777670

    Open questions at the time
    • Did not quantify residual monomer activity in vivo
    • Single truncating allele
  4. 2007 Medium

    Showed a frameshift removing the dimerization cysteine yields monomeric OPG yet still elevated circulating immunoreactive protein, clarifying that immunoassay levels do not reflect functional activity.

    Evidence Sequencing plus longitudinal serum OPG and soluble RANKL ELISA in a patient

    PMID:17352649

    Open questions at the time
    • Dimerization inferred from sequence, not re-tested directly
    • Single patient
  5. 2011 High

    Identified functional cis-regulatory variants controlling OPG transcription and splicing, extending genetic risk beyond coding mutations.

    Evidence Promoter-luciferase reporter in three cell lines and an exon-trapping splicing assay

    PMID:21994215

    Open questions at the time
    • Effect on endogenous OPG protein levels in bone not measured
    • Trans-acting factors driving promoter activity unidentified
  6. 2013 Medium

    Defined an upstream regulatory axis for OPG production in tumor cells, implicating membrane-bound TNF-α/TNFR1 signaling.

    Evidence Characterization of OPG production in melanoma cell lines with pathway dissection

    PMID:23490134

    Open questions at the time
    • Limited methodological detail
    • Functional consequence of tumor OPG not established here
  7. 2014 Medium

    Initially characterized a read-through allele as gain-of-function with enhanced osteoclastogenesis inhibition causing early-onset OA with chondrocalcinosis.

    Evidence Cell-based bone resorption assay comparing mutant vs. wild-type OPG, with exome sequencing and linkage

    PMID:24743232

    Open questions at the time
    • Single assay type
    • Mechanism linking enhanced inhibition to chondrocalcinosis unexplained
  8. 2015 Medium

    Placed OPG transcription under circadian control, linking α1B-adrenergic signaling and clock genes to rhythmic bone gene expression.

    Evidence Gain/loss-of-function in MC3T3-E1 cells, phenylephrine stimulation, and α1B-AR knockout mice

    PMID:26453621

    Open questions at the time
    • Direct promoter occupancy by Bmal1/REV-ERBα not shown
    • Physiological consequence for bone mass not quantified
  9. 2016 Medium

    Identified miR-145 as a direct post-transcriptional repressor of TNFRSF11B in chondrocytes affecting proliferation and fibrosis.

    Evidence Dual-luciferase reporter, miR-145 mimic, and TNFRSF11B siRNA phenocopy in chondrocytes

    PMID:27922673

    Open questions at the time
    • In vivo relevance not established
    • Single cell type
  10. 2020 Medium

    Revealed a non-canonical, RANKL-independent OPG function: direct binding and phosphorylation of GSK-3β to activate Wnt/β-catenin signaling in gastric cancer.

    Evidence Co-IP of OPG–GSK-3β, immunofluorescence for nuclear β-catenin, and functional cancer assays

    PMID:32398963

    Open questions at the time
    • Single Co-IP without reciprocal/structural validation
    • How a secreted decoy accesses cytoplasmic GSK-3β unresolved
  11. 2021 High

    Reclassified the OPG-XL read-through allele as loss-of-function for RANKL-mediated osteoclastogenesis with reduced binding to osteoblastic cells, overturning the earlier gain-of-function model.

    Evidence Recombinant OPG-XL vs. wild-type in osteoclastogenesis monoculture/coculture, survival, apoptosis, and binding assays

    PMID:33559312

    Open questions at the time
    • Mechanism connecting reduced binding to chondrocalcinosis phenotype unresolved
    • Effect on TRAIL/survival unchanged, leaving disease driver partly open
  12. 2021 Medium

    Demonstrated OPG drives chondrocyte-to-osteoblast transition in articular cartilage through pathways independent of the RANK/RANKL triad.

    Evidence Lentiviral TNFRSF11B overexpression in primary chondrocytes in a 3D chondrogenesis model with RT-qPCR, IHC, and mineralization assays

    PMID:33989379

    Open questions at the time
    • Downstream effector pathway in cartilage not identified
    • Receptor/binding partner mediating the effect unknown
  13. 2021 Low

    Implicated TAp63 as a transcriptional regulator of TNFRSF11B in bone remodeling.

    Evidence Implied transcriptional regulation study (abstract stub)

    PMID:34763601

    Open questions at the time
    • No experimental detail available to assess rigor
    • Direct promoter binding not demonstrated
  14. 2024 Medium

    Placed OPG's pro-tumor activity in bladder cancer downstream of PI3K/AKT signaling via inhibitor rescue.

    Evidence Knockdown/overexpression in bladder cancer cells with LY294002 rescue, EMT markers, and in vivo tumor assay

    PMID:39481664

    Open questions at the time
    • No direct binding partner for pathway activation identified
    • Single lab, no structural data
  15. 2025 Medium

    Showed OPG overexpression suppresses osteoclastogenesis but does not promote osteogenesis, and identified secreted proteomic mediators associated with osteoclast inhibition.

    Evidence Lentiviral overexpression in UCMSCs, conditioned medium osteoclast/osteogenic assays, and conditioned-medium proteomics

    PMID:40380204

    Open questions at the time
    • Causal role of identified proteins (C1R, FETUB, METRNL) not tested
    • Single cell model
  16. 2026 High

    Provided in vivo causal confirmation that the TNFRSF11B mutation is loss-of-function, driving osteopenia, increased osteoclastogenesis, and CPPD-related joint pathology.

    Evidence CRISPR/Cas9 knock-in mouse with histology, bone remodeling and osteoclast assays, and CPPD biomarker measurement

    PMID:41826214

    Open questions at the time
    • Molecular link from OPG loss to pyrophosphate/ENPP1 elevation not fully resolved
    • Sex-specific OA penetrance unexplained

Open questions

Synthesis pass · forward-looking unresolved questions
  • The receptor and downstream effector pathway mediating OPG's RANKL-independent actions in cartilage and tumors remain undefined.
  • No cell-surface receptor for non-canonical OPG signaling identified
  • Structural basis for OPG–GSK-3β interaction unknown
  • Reconciliation of decoy versus signaling roles incomplete

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3 GO:0140313 molecular sequestering activity 2
Localization
GO:0005576 extracellular region 2
Pathway
R-HSA-1643685 Disease 3 R-HSA-1266738 Developmental Biology 2 R-HSA-162582 Signal Transduction 2
Partners
GSK-3ΒRANKL

Evidence

Reading pass · 16 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 A 3-bp in-frame deletion in TNFRSF11B (loss of an aspartate residue) results in a mutant OPG protein that fails to suppress bone resorption in vitro, establishing this as an inactivating mutation. Wild-type OPG expressed in human epithelial kidney cells and collected from conditioned medium suppressed bone resorption, whereas the mutant form did not. Recombinant wild-type and mutant OPG cDNA expression in human epithelial kidney cells, conditioned medium collection, in vitro bone resorption assay Human molecular genetics High 12189164
2003 Mutations in the cysteine-rich ligand-binding domain of OPG (encoded by TNFRSF11B) disrupt binding to RANKL. Missense mutations at cysteine residues cause the most severe phenotype (predicted major disruption to ligand-binding), while non-cysteine missense mutations in the same domain cause intermediate phenotype, and a C-terminal insertion/deletion causes the mildest phenotype, establishing a genotype-phenotype correlation linked to the degree of RANKL-binding disruption. Mutation analysis of TNFRSF11B in affected families, predicted structural effects on OPG ligand-binding domain correlated with clinical phenotype severity Journal of bone and mineral research Medium 14672344
2005 A truncating mutation in TNFRSF11B (homozygous insertion/deletion in exon 5, truncating protein at amino acid 325) eliminates the C-terminal domain, abolishes OPG homodimerization, and decreases the capacity of mutant OPG to bind RANKL, as confirmed by Western blotting and ELISA after transient overexpression. Transient overexpression of mutant OPG, Western blotting for homodimerization, ELISA for RANKL-binding capacity Bone High 15777670
2007 The TNFRSF11B 'Balkan' mutation (966_969delTGACinsCTT) causes a frameshift that deletes 79 C-terminal amino acids from the OPG monomer, including a cysteine residue required for homodimerization, resulting in truncated monomeric OPG that cannot form homodimers yet is still detectable as elevated circulating immunoreactive OPG along with elevated soluble RANKL. TNFRSF11B sequencing, serum immunoreactive OPG and soluble RANKL ELISA measurement over 4 years Journal of bone and mineral research Medium 17352649
2011 The T allele of the C950T (rs2073617) promoter polymorphism in TNFRSF11B drives lower luciferase reporter expression in HeLa, COS-7, and RAW264.7 cell lines compared to the C allele, indicating a functional cis-regulatory effect on OPG transcription. Additionally, the C allele of rs4876869 causes exon skipping in a pre-mRNA splicing assay, reducing full-length OPG transcript. Promoter-luciferase reporter assay in three cell lines; exon-trapping splicing assay for rs4876869 Journal of molecular endocrinology High 21994215
2013 Human metastatic melanomas constitutively produce OPG (TNFRSF11B product) through a mechanism governed by membrane-bound TNF-α signaling through TNF receptor 1 (TNFR1), defining a specific regulatory axis controlling OPG production in tumor cells. Characterization of OPG production by melanoma cell lines; identification of membrane-bound TNF-α/TNFR1 signaling as the regulating mechanism Pigment cell & melanoma research Medium 23490134
2014 A heterozygous read-through mutation (c.1205A>T; p.Stop402Leu) in TNFRSF11B results in a gain-of-function OPG with enhanced capacity to inhibit osteoclastogenesis and bone resorption in a cell-based bone resorption assay, causing familial early-onset OA with chondrocalcinosis. Cell-based bone resorption assay comparing mutant vs. wild-type OPG; exome sequencing and linkage analysis for mutation identification Annals of the rheumatic diseases Medium 24743232
2015 Circadian expression of Tnfrsf11b (OPG) in osteoblasts is regulated by the clock genes Bmal1 and REV-ERBα (Nr1d1): Bmal1 positively regulates rhythmic Tnfrsf11b expression and REV-ERBα negatively regulates it. α1B-adrenergic receptor signaling controls this circadian regulation, as genetic ablation of α1B-AR alters Tnfrsf11b expression concomitant with Bmal1 and Per2 in bone. Loss-of-function and gain-of-function experiments in MC3T3-E1 osteoblast cells; pharmacological stimulation with phenylephrine (α1-AR agonist); genetic ablation of α1B-AR in mice with in vivo bone expression analysis Biology open Medium 26453621
2016 TNFRSF11B is a direct target of miR-145 in chondrocytes, as confirmed by dual-luciferase reporter assay. miR-145 overexpression suppresses TNFRSF11B expression and inhibits chondrocyte proliferation and fibrosis; siRNA knockdown of TNFRSF11B phenocopies this inhibition. Dual-luciferase reporter assay for miR-145 targeting; miR-145 mimic transfection; siRNA knockdown of TNFRSF11B; MTT proliferation assay; Western blot for fibrosis markers Molecular medicine reports Medium 27922673
2020 TNFRSF11B (OPG) directly binds GSK-3β and upregulates its phosphorylation, leading to increased nuclear β-catenin and activation of Wnt/β-catenin downstream effectors in gastric cancer cells, promoting proliferation, migration, invasion, and inhibiting apoptosis. Co-immunoprecipitation (TNFRSF11B–GSK-3β interaction); immunofluorescence for nuclear β-catenin; Western blot for β-catenin and downstream effectors; in vitro and in vivo functional assays (proliferation, migration, invasion, apoptosis) International journal of biological sciences Medium 32398963
2021 The OPG-XL (read-through/gain-of-function) mutation in TNFRSF11B is actually a loss-of-function mutation with respect to RANKL-mediated osteoclastogenesis: recombinant OPG-XL is less effective than wild-type OPG at blocking RANKL-induced osteoclastogenesis in monoculture and coculture models, and significantly less OPG-XL binds to osteoblastic cells. Effects on osteoclast survival and TRAIL-induced apoptosis were similar to wild-type OPG. In vitro RANKL-induced osteoclastogenesis in monoculture and coculture; osteoclast survival assay; TRAIL-induced apoptosis assay; ELISA and flow cytometry for OPG binding to MC3T3-E1 osteoblastic cells Arthritis & rheumatology High 33559312
2021 Overexpression of TNFRSF11B in primary human articular chondrocytes in a 3D in vitro chondrogenesis model strongly upregulates MMP13, COL2A1, COL1A1, and osteoblast markers RUNX2, ASPN, and OGN, and increases mineralization, suggesting OPG drives chondrocyte-to-osteoblast transition in OA. Notably, RANK and RANKL expression remained unchanged, indicating downstream pathways in cartilage independent of the OPG/RANK/RANKL triad. Lentiviral overexpression of TNFRSF11B in primary chondrocytes; 3D chondrogenic culture model; RT-qPCR; immunohistochemistry; ELISA; Alcian blue staining; RNA-seq correlation analysis Rheumatology (Oxford, England) Medium 33989379
2021 TAp63 regulates bone remodeling by modulating the expression of TNFRSF11B/osteoprotegerin. Not fully detailed in abstract; implied transcriptional regulation study Cell cycle Low 34763601
2024 TNFRSF11B promotes bladder cancer cell proliferation, migration, invasion, and EMT, and inhibits apoptosis via activation of the PI3K/AKT pathway; inhibition of PI3K/AKT with LY294002 reverses the effects of TNFRSF11B overexpression. siRNA knockdown and overexpression of TNFRSF11B in bladder cancer cells; Western blot for PI3K/AKT pathway markers and EMT markers; cell proliferation, migration, and invasion assays; apoptosis assay; in vivo tumor assay; LY294002 pharmacological inhibition Molecular and cellular probes Medium 39481664
2025 TNFRSF11B overexpression in UCMSCs suppresses RANKL-induced osteoclast differentiation (via conditioned medium), but neither overexpression of TNFRSF11B nor treatment with exogenous OPG protein enhances osteogenic differentiation of UCMSCs in vitro. Proteomic analysis of conditioned medium from TNFRSF11B-overexpressing UCMSCs identified downregulation of C1R, MDH1, and ACLY and upregulation of FETUB and METRNL, associated with osteoclast inhibition. Lentiviral overexpression in UCMSCs; conditioned medium treatment of osteoclast precursors; ALP staining; TRAP staining; qRT-PCR; proteomic analysis Journal of orthopaedic surgery and research Medium 40380204
2026 CRISPR/Cas9 knock-in of the TNFRSF11B mutation (OPGmt) in mice produces osteopenia, elevated bone remodeling markers, increased osteoclast numbers and activity, and in female homozygous mice, osteoarthritis features (articular cartilage loss) by 12 months. Joints of OPGmt mice showed elevated pyrophosphate, TGF-β1, and ENPP1 activity — biomarkers of CPPD disease — establishing the mutation as a loss-of-function driving increased osteoclastogenesis and CPPD-related joint pathology. CRISPR/Cas9 knock-in murine model; histological scoring (Mankin); bone remodeling biomarkers; osteoclast number/activity assays; CPPD biomarker measurement (pyrophosphate, TGF-β1, ENPP1 activity) at 6 and 12 months Annals of the rheumatic diseases High 41826214

Source papers

Stage 0 corpus · 46 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 A mutation in the gene TNFRSF11B encoding osteoprotegerin causes an idiopathic hyperphosphatasia phenotype. Human molecular genetics 165 12189164
2003 Idiopathic hyperphosphatasia and TNFRSF11B mutations: relationships between phenotype and genotype. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 87 14672344
2011 Assessment of the genetic effects of polymorphisms in the osteoprotegerin gene, TNFRSF11B, on serum osteoprotegerin levels and carotid plaque vulnerability. Stroke 54 21903966
2014 A gain of function mutation in TNFRSF11B encoding osteoprotegerin causes osteoarthritis with chondrocalcinosis. Annals of the rheumatic diseases 48 24743232
2007 Identification of sex-specific associations between polymorphisms of the osteoprotegerin gene, TNFRSF11B, and Paget's disease of bone. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 46 17388729
2020 TNFRSF11B activates Wnt/β-catenin signaling and promotes gastric cancer progression. International journal of biological sciences 42 32398963
2005 TNFRSF11B gene variants and bone mineral density in postmenopausal women in Malta. Maturitas 40 16343827
2012 Association between TNFRSF11B gene polymorphisms and history of ischemic stroke in Italian diabetic patients. Human genetics 37 22965192
2011 Functional polymorphisms within the TNFRSF11B (osteoprotegerin) gene increase the risk for low bone mineral density. Journal of molecular endocrinology 37 21994215
2005 An intermediate form of juvenile Paget's disease caused by a truncating TNFRSF11B mutation. Bone 28 15777670
2014 Denosumab treatment for juvenile Paget's disease: results from two adult patients with osteoprotegerin deficiency ("Balkan" mutation in the TNFRSF11B gene). The Journal of clinical endocrinology and metabolism 27 24433001
2014 TNFRSF11B gene polymorphisms increased risk of peripheral arterial occlusive disease and critical limb ischemia in patients with type 2 diabetes. Acta diabetologica 27 25323324
2007 Juvenile Paget's disease: the second reported, oldest patient is homozygous for the TNFRSF11B "Balkan" mutation (966_969delTGACinsCTT), which elevates circulating immunoreactive osteoprotegerin levels. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 26 17352649
2022 The role of TNFRSF11B in development of osteoarthritic cartilage. Rheumatology (Oxford, England) 25 33989379
2011 TNFRSF11B gene polymorphisms 1181G > C and 245T > G as well as haplotype CT influence bone mineral density in postmenopausal women. Maturitas 23 21411255
2013 Juvenile paget's disease in an Iranian kindred with vitamin D deficiency and novel homozygous TNFRSF11B mutation. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 22 23322328
2012 Genotype-phenotype correlation in juvenile Paget disease: role of molecular alterations of the TNFRSF11B gene. Endocrine 20 22638612
2014 Novel homozygous mutations in the osteoprotegerin gene TNFRSF11B in two unrelated patients with juvenile Paget's disease. Bone 19 25108083
2010 TNFRSF11B computational development network construction and analysis between frontal cortex of HIV encephalitis (HIVE) and HIVE-control patients. Journal of inflammation (London, England) 19 20920282
2016 Effects of miR-145 on the inhibition of chondrocyte proliferation and fibrosis by targeting TNFRSF11B in human osteoarthritis. Molecular medicine reports 17 27922673
2014 TNFRSF11B gene polymorphisms, bone mineral density, and fractures in Slovak postmenopausal women. Journal of applied genetics 15 25323794
2013 Differential expression and tumor necrosis factor-mediated regulation of TNFRSF11b/osteoprotegerin production by human melanomas. Pigment cell & melanoma research 14 23490134
2017 Polymorphism rs2073618 of the TNFRSF11B (OPG) Gene and Bone Mineral Density in Mexican Women with Rheumatoid Arthritis. Journal of immunology research 12 28758134
2013 Polymorphism of LRP5, but not of TNFRSF11B, is associated with a decrease in bone mineral density in postmenopausal Maya-Mestizo women. American journal of human biology : the official journal of the Human Biology Council 11 24130145
2021 Effects of the TNFRSF11B Mutation Associated With Calcium Pyrophosphate Deposition Disease in Osteoclastogenesis in a Murine Model. Arthritis & rheumatology (Hoboken, N.J.) 10 33559312
2015 α1B-Adrenergic receptor signaling controls circadian expression of Tnfrsf11b by regulating clock genes in osteoblasts. Biology open 9 26453621
2018 Effects of osteoprotegerin/TNFRSF11B in two models of abdominal aortic aneurysms. Molecular medicine reports 8 29749489
2021 Association between Polymorphisms in the IL-1β, TNFRSF11B, CASP1, and IL-6 Genes and Orthodontic-Induced External Apical Root Resorption. Journal of clinical medicine 6 34575287
2021 Associations of osteoprotegerin (OPG) TNFRSF11B gene polymorphisms with risk of fractures in older adult populations: meta-analysis of genetic and genome-wide association studies. Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA 6 34716467
2018 Significant Association between OPG/TNFRSF11B Variant and Common Complex Ischemic Stroke. Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association 6 29501268
2019 Juvenile Paget's disease with compound heterozygous mutations in TNFRSF11B presenting with recurrent clavicular fractures and a mild skeletal phenotype. Bone 5 31655221
2011 TNFRSF11B gene haplotype and its association with bone mineral density variations in postmenopausal Mexican-Mestizo women. Maturitas 5 22079369
2024 TNFRSF11B promotes the progression of bladder cancer through PI3K/AKT signaling pathway. Molecular and cellular probes 4 39481664
2021 TAp63 regulates bone remodeling by modulating the expression of TNFRSF11B/Osteoprotegerin. Cell cycle (Georgetown, Tex.) 4 34763601
2014 Exclusion of TNFRSF11B as Candidate Gene for Otosclerosis in Campania Population. Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India 4 25032118
2019 [Association between TNFRSF11A and TNFRSF11B gene polymorphisms and the outcome of hepatitis C virus infection]. Zhonghua liu xing bing xue za zhi = Zhonghua liuxingbingxue zazhi 3 31658533
2025 TNFRSF11B-modified umbilical cord mesenchymal stem cells as a novel strategy for bone-related diseases by suppressing osteoclast activity. Journal of orthopaedic surgery and research 2 40380204
2025 Juvenile Paget disease with unique compound heterozygous sequence variants in the TNFRSF11B gene. Orphanet journal of rare diseases 1 40775369
2023 Establishment of a TNFRSF11B knock-out human induced pluripotent stem cell line (KSCBi002-B-2) via CRISPR/Cas9 system. Stem cell research 1 37481965
2021 Juvenile Paget's Disease: Report of a successful treatment throughout the complete growth of a patient with a missense TNFRSF11B mutation. Joint bone spine 1 34166796
2026 TNFRSF11B modulates Marek's disease virus infection by regulating apoptosis in chicken embryo fibroblasts. Frontiers in veterinary science 0 41728123
2026 A novel murine model of early calcium pyrophosphate deposition disease based on the TNFRSF11B mutation mimics features of the human disease. Annals of the rheumatic diseases 0 41826214
2026 The first neonatal case of Juvenile Paget disease with homozygous deletion in the TNFRSF11B gene. Journal of pediatric endocrinology & metabolism : JPEM 0 42112796
2025 [Association of TNFRSF11B gene rs2073618 and rs3102735 polymorphisms with susceptibility to Gastric cancer]. Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 0 40623930
2025 The Influence of Clinical Factors and Genetic Variants of COL1A1 and TNFRSF11B on Bone Mineral Density in Postmenopausal Women. International journal of molecular sciences 0 41009461
2013 TNFRSF11B polymorphisms are associated with metabolic traits in Uyghur and Han ethnic groups. Endocrine research 0 23772656

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