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anti-Human TNFSF11 Antibodies:
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Human Monoclonal TNFSF11 Primary Antibody for ChIP, FACS - ABIN252476
Kikuchi, Matsuguchi, Tsuboi, Mitani, Tanaka, Matsuoka, Yamamoto, Hishikawa, Noguchi, Yoshikai: Gene expression of osteoclast differentiation factor is induced by lipopolysaccharide in mouse osteoblasts via Toll-like receptors. in Journal of immunology (Baltimore, Md. : 1950) 2001
Show all 21 Pubmed References
Human Polyclonal TNFSF11 Primary Antibody for IF (p), IHC (p) - ABIN672696
Yang, Li, Yang, Shen, Zou, Zhu, Zhang, Yang, Li: Efficacy and safety of echinacoside in a rat osteopenia model. in Evidence-based complementary and alternative medicine : eCAM 2013
Show all 15 Pubmed References
Human Polyclonal TNFSF11 Primary Antibody for IF (p), IHC (p) - ABIN668556
Zhang, Liu, Li, Bai: Mycobacterium tuberculosis 10-kDa co-chaperonin regulates the expression levels of receptor activator of nuclear factor-?B ligand and osteoprotegerin in human osteoblasts. in Experimental and therapeutic medicine 2015
Show all 11 Pubmed References
Human Monoclonal TNFSF11 Primary Antibody for ChIP, CyTOF - ABIN252546
Hsu, Lacey, Dunstan, Solovyev, Colombero, Timms, Tan, Elliott, Kelley, Sarosi, Wang, Xia, Elliott, Chiu, Black, Scully, Capparelli, Morony, Shimamoto, Bass, Boyle: Tumor necrosis factor receptor family member RANK mediates osteoclast differentiation and activation induced by osteoprotegerin ligand. in Proceedings of the National Academy of Sciences of the United States of America 1999
Show all 11 Pubmed References
Mouse (Murine) Monoclonal TNFSF11 Primary Antibody for IHC (fro), FACS - ABIN2479510
Andersen, Jørgensen, Bardram, Hilsted: Screening for multiple endocrine neoplasia type 1 in patients with recognized pituitary adenoma. in Clinical endocrinology 1991
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Human Monoclonal TNFSF11 Primary Antibody for FACS, IHC (fro) - ABIN252684
Yoneda, Ishimaru, Arakaki, Kobayashi, Izawa, Moriyama, Hayashi: Estrogen deficiency accelerates murine autoimmune arthritis associated with receptor activator of nuclear factor-kappa B ligand-mediated osteoclastogenesis. in Endocrinology 2004
Show all 3 Pubmed References
Human Monoclonal TNFSF11 Primary Antibody for CyTOF, FACS - ABIN4361916
Shetty, Pepin, Charest, Perron, Doyle, Voisine, Dagenais, Pibarot, Mathieu: Expression of bone-regulatory proteins in human valve allografts. in Heart (British Cardiac Society) 2006
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Human Polyclonal TNFSF11 Primary Antibody for IHC (p), WB - ABIN541285
Kong, Yoshida, Sarosi, Tan, Timms, Capparelli, Morony, Oliveira-dos-Santos, Van, Itie, Khoo, Wakeham, Dunstan, Lacey, Mak, Boyle, Penninger: OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node organogenesis. in Nature 1999
Show all 3 Pubmed References
Mouse (Murine) Polyclonal TNFSF11 Primary Antibody for ELISA, WB - ABIN4886751
Wei, Wang, Gong, Zeng: Effectiveness of combined salmon calcitonin and aspirin therapy for osteoporosis in ovariectomized rats. in Molecular medicine reports 2016
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Changes in the RANKL/RANK/OPG axis levels in cerebrospinal fluid are associated with clinical onset of multiple sclerosis.
Higher pre-diagnosis endogenous concentrations of the decoy receptor for RANKL, OPG, appear to increase risk of death after a breast cancer diagnosis especially in those diagnosed with ER+ disease.
RANK/RANKL were identified as crucial regulators for BRCA1 mutation-driven breast cancer. Current prevention strategies for BRCA1 mutation carriers are associated with wide-ranging risks; therefore, the search for alternative, non-invasive strategies is of paramount importance
High RANKL expression is associated with gastric cancer cell migration.
A high level of sRANKL in bronchoalveolar lavage fluid of non-small cell lung cancer patients may predict worse survival.
RANKL/OPG ratio was significantly higher in the prolactinoma group than in the control group.
RANKL mRNA expression was higher in tumour tissue from patients with metastatic prostate cancer compared to local disease. The RANKL/OPG ratio was low in normal prostate tissue and high in tumours with bone metastases. Expression was high in BPH tissue but did not exceed as much as in the tumour tissue.
In cardiovascular risks, OPG serum level might increase as a preventive compensatory mechanism to neutralize the RANKL level increment. The determination of the OPG-RANKL system is a diagnostic indicator for the intensity of vascular calcification and atherosclerosis in SSc patients.
sRANKL and OPG may play a role in the pathogenesis of diabetes as well as metabolic disturbance
regulation of OSCAR by TNF-alpha and receptor activator of NF kappa beta ligand (RANKL) in pre-osteoclasts/osteoclasts
The -643C>T RANKL polymorphism, through its significant influence on body weight and BMI value, may contribute to the development of Osteoporosis in Postmenopausal women.
In the present study, we measured expression of RANKL in human periosteum-derived cells(hPDCs) undergoing osteoblastic differentiation and found that expression of RANKL mRNA was markedly increased in these cells in a time-dependent manner.RANKL protein expression was also significantly enhanced in osteogenic-conditioned media from hPDCs undergoing osteoblastic differentiation
MiR-217 is a useful diagnostic biomarker and is involved in human podocyte cells apoptosis via targeting TNFSF11 in membranous nephropathy.
rs9525641 might contribute to bone mineral density
Vascular smooth cells are a significant source of osteoprotegerin within the vasculature but that RANKL, once present, downregulates this production and appears capable of preventing the "protective" upregulation of OPG seen with VSMCs exposed to physiological levels of cyclic strain.
receptor activator for nuclear factor-kappa B ligand (RANKL), secreted by human embryonic trophoblasts and maternal decidual stromal cells, polarizes decidual macrophages toward a M2 phenotype.
There were no significant associations involving the RANKL gene. Thus, it is suggested that alterations in the OPG and RANK genes are primarily responsible for altering the function and expression of the RANKL ligand, resulting in a predisposition to chronic arthralgia and comorbid temporomandibular OA.
Vitamin D, tumor necrosis factor (TNF)-alpha, receptor activator of nuclear factor-KB ligand (RANKL), and OPG levels were determined in GCF and serum. Baseline clinical parameters were similar in all periodontitis groups (P > 0.05) but were higher than that in controls
study demonstrated the association of the -643C > T polymorphism with bone mineral density variation and osteoporosis risk in postmenopausal Tunisian women
down-regulated miR-143-5p promotes the differentiation of DPSCs into odontoblasts by enhancing Runx2 expression via the OPG/RANKL signaling pathway.
results suggest that central administration of RANKL reduces food intake and causes weight loss via modulating the hypothalamic NPY/CART pathways.
MMP14 is a novel target of PTH signaling in osteocytes that controls resorption by regulating soluble RANKL production.
The results demonstrate that the membrane-bound form of RANKL is sufficient for most functions of this protein but that the soluble form does contribute to physiological bone remodeling in adult mice.
lactation increases physiological maxillary bone remodeling and orthodontic tooth movement, and both require activation of RANK/RANKL/OPG system
although TNFalpha does not induce osteoclastogenesis alone, it does work with RANKL to induce osteoclastic differentiation, and the NFkappaB pathway may serve an important role in this process.
the investigation of RANK and RANKL as possible novel immunotherapy targets in cancer is a rational approach. Here we have defined the mechanism of action of RANKL-RANK blockade in combination with anti-CTLA4, and provide insight into the combination efficacy observed in the case reports.
the molecular level, we confirmed, for the first time, that RES upregulated FoxO1 transcriptional activity by inhibiting the PI3K/AKT signaling pathway, and hence promoted resistance to oxidative damage and restrained osteoclastogenesis. Inhibition of the PI3K/AKT signaling pathway may be induced by RANKL.
Deletion of the RANKL D5 enhancer delays the progression of atherosclerotic plaque development and plaque calcification in hypercholesterolemic mice.
these results suggest that A2BAR stimulation inhibits the activation of ERK1/2, p38 and NF-kappaB by RANKL, which suppresses the induction of osteoclast marker genes, thus contributing to the decrease in osteoclast cell-cell fusion and bone resorption activity.
CD11b promotes the differentiation of osteoclasts induced by RANKL through the Syk signaling pathway.
RANKL and Src has an unrecognized role in osteocyte survival.
compressive force induced the differentiation of RAW264.7 from increase in RANK and decrease in LGR4 expression.
miR-145 expression was inhibited in RANKL-induced osteoclastogenesis
LPS increased mRNA and protein expressions of IL-6 and RANKL on day 14
hBD-1 potentiates the induction of in vitro osteoclastogenesis by RANKL via enhanced phosphorylation of the p44/42 MAPKs
findings indicate that STAT5 contributes to the remarkable IL-3-mediated inhibition of RANKL-induced osteoclastogenesis by activating Id genes and their associated pathways.
In conclusion, the results suggest that linarin has anti-osteoclastic effects and may serve as potential modulatory agents for the prevention and treatment of bone loss-associated diseases.
RANKL/RANK control progenitor cell expansion and tumorigenesis in inherited breast cancer.
Rankl(-/-) bone marrow-mesenchymal stromal cell displayed reduced clonogenicity and osteogenic capacity.
In this study, the authors identified by gene expression profiling that microgravity induces high levels of TRAIL expression in murine preosteoclast cells in the absence of RANKL stimulation compared to ground based cultures.
This gene encodes a member of the tumor necrosis factor (TNF) cytokine family which is a ligand for osteoprotegerin and functions as a key factor for osteoclast differentiation and activation. This protein was shown to be a dentritic cell survival factor and is involved in the regulation of T cell-dependent immune response. T cell activation was reported to induce expression of this gene and lead to an increase of osteoclastogenesis and bone loss. This protein was shown to activate antiapoptotic kinase AKT/PKB through a signaling complex involving SRC kinase and tumor necrosis factor receptor-associated factor (TRAF) 6, which indicated this protein may have a role in the regulation of cell apoptosis. Targeted disruption of the related gene in mice led to severe osteopetrosis and a lack of osteoclasts. The deficient mice exhibited defects in early differentiation of T and B lymphocytes, and failed to form lobulo-alveolar mammary structures during pregnancy. Two alternatively spliced transcript variants have been found.
TNF-related activation-induced cytokine
, osteoclast differentiation factor
, osteoprotegerin ligand
, receptor activator of nuclear factor kappa B ligand
, receptor activator of nuclear factor kappa-B ligand
, tumor necrosis factor ligand superfamily member 11
, tumor necrosis factor (ligand) superfamily, member 11
, Receptor activator of nuclear factor kappa-B ligand
, OPG ligand
, receptor activator of NF-kappaB ligand
, tumor necrosis factor-related activation-induced cytokine
, TNF superfamily member 11 L homeolog
, tumor necrosis factor superfamily member 11 L homeolog