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Human Monoclonal TNFRSF11A Primary Antibody for CyTOF, FACS - ABIN252472
Fiumara, Snell, Li, Mukhopadhyay, Younes, Gillenwater, Cabanillas, Aggarwal, Younes: Functional expression of receptor activator of nuclear factor kappaB in Hodgkin disease cell lines. in Blood 2001
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Human Monoclonal TNFRSF11A Primary Antibody for FACS, IHC (p) - ABIN252036
Lee, Kim, Jun, Yoo, Woo, Choi, Lee, Song, Sohn, Park-Min, Ivashkiv, Ji: Direct inhibition of human RANK+ osteoclast precursors identifies a homeostatic function of IL-1beta. in Journal of immunology (Baltimore, Md. : 1950) 2010
Show all 10 Pubmed References
Human Monoclonal TNFRSF11A Primary Antibody for CyTOF, ELISA (Capture) - ABIN4900544
Vernal, Dutzan, Hernández, Chandía, Puente, León, García, Del Valle, Silva, Gamonal: High expression levels of receptor activator of nuclear factor-kappa B ligand associated with human chronic periodontitis are mainly secreted by CD4+ T lymphocytes. in Journal of periodontology 2006
Show all 6 Pubmed References
Mouse (Murine) Monoclonal TNFRSF11A Primary Antibody for FACS, IP - ABIN2479562
García-Pérez, Noguera, Hermenegildo, Martínez-Romero, Tarín, Cano: Alterations in the phenotype and function of immune cells in ovariectomy-induced osteopenic mice. in Human reproduction (Oxford, England) 2006
Human Monoclonal TNFRSF11A Primary Antibody for FACS - ABIN4897927
Riegel, Maurer, Prior, Stegmaier, Heppert, Wagner, Hänsch: Human polymorphonuclear neutrophils express RANK and are activated by its ligand, RANKL. in European journal of immunology 2012
Insulin induces RANK expression via ERK1/2, which contributes to the enhancement of osteoclast differentiation.
This indicated that RANK might be the binding target of baicalin. In sum, our findings revealed baicalin increased osteoclast maturation and function via p-ERK (show EPHB2 Antibodies)/Mitf (show MITF Antibodies) signalling. In addition, the results suggest that baicalin can potentially be used as a natural product for the treatment of bone fracture
RANKL (show TNFSF11 Antibodies)/RANK control progenitor cell expansion and tumorigenesis in inherited breast cancer.
Artesunate inhibits RANKL (show TNFSF11 Antibodies)-induced osteoclastogenesis by suppressing the NF-kappaB (show NFKB1 Antibodies) signaling pathway.
Data suggest that mutations at position I248 in DE-loop of murine RANKL (show TNFSF11 Antibodies) have effects on interaction of RANKL (show TNFSF11 Antibodies) with RANK and on subsequent activation of osteoclastogenesis by this hetero-multimer. (RANKL (show TNFSF11 Antibodies) = osteoclast differentiation factor (show TNFSF11 Antibodies); RANK = tumor necrosis factor (show TNF Antibodies) receptor superfamily, member 11a protein)
The persistence of bone erosion and synovial osteoclasts in Rank-deficient mice, and the ability of TNF (show TNF Antibodies)/IL-6 (show IL6 Antibodies) to induce osteoclastogenesis, suggest that more than one cytokine pathway exists to generate these bone-resorbing cells in inflamed joints.
Muscle RANK deletion had no significant effects on the sham or denervated slow-twitch soleus muscles. These data identify a novel role for RANK as a key regulator of Ca(2 (show CA2 Antibodies)+)storage and SERCA (show ATP2A3 Antibodies) activity, ultimately affecting denervated skeletal muscle function.
present study shows that ginsenoside Rg3 protects against LPS (show TLR4 Antibodies)-induced acute lung injury through inactivating the NF-kappaB (show NFKB1 Antibodies) signaling
In palmatine-treated mice, RANKL (show TNFSF11 Antibodies) and OPG (show TNFSF11 Antibodies) expression decreased. In the culture supernatant of MC3T3-E1 cells, RANKL (show TNFSF11 Antibodies) and OPG (show TNFSF11 Antibodies) levels were significantly reduced by palmatine addition.
Results show that moderate increases in affinity for RANK lead to a substantial augmentation of osteoclast formation, signaling, and bone resorption suggesting a biphasic relationship between RANKL (show TNFSF11 Antibodies)/RANK affinity and osteoclastogenic capacity.
For the RANK gene, the AGTGC haplotype was associated with the lowest risk of presenting chronic joint pain in individuals without TMD (show TTN Antibodies) (P=0.03). This study supports the hypothesis that changes in the OPG (show TNFRSF11B Antibodies) and RANK genes influence the presence of chronic joint pain in individuals with and without TMD (show TTN Antibodies).
In this study, whole exome sequencing (WES) was successfully used in six patients with malignant infantile osteopetrosis (show CSF1 Antibodies) (MIOP) and identified mutations in four MIOP-related genes (CLCN7 (show CLCN7 Antibodies), TCIRG1 (show TCIRG1 Antibodies), SNX10 (show SNX10 Antibodies), and TNFRSF11A).
triple-negative breast cancer (TNBC) patients that expressed both RANK and RANKL (show TNFSF11 Antibodies) proteins had significantly worse RFS and OS than patients with RANK-positive, RANKL (show TNFSF11 Antibodies)-negative tumors. RANKL (show TNFSF11 Antibodies) was an independent, poor prognostic factor for RFS and OS in multivariate analysis in samples that expressed both RANK and RANKL (show TNFSF11 Antibodies).
RANK is increased in hormone receptor (show NR4A1 Antibodies) negative and basal breast cancer, and correlates with worse recurrence-free survival and risk of bone metastasis.
Studies showed that the central hypothalamic-pituitary regulatory system, via it's relative hormones, seems to control OPG/RANKL (show TNFSF11 Antibodies)/RANK system function, and the pulsatility and circadian rhythmicity of these hormones may induce an oscillatory fluctuation of the OPG/ RANKL (show TNFSF11 Antibodies) ratio. Also, psycological characteristics may provoke a shift of the OPG/ RANKL (show TNFSF11 Antibodies) ratio towards an unbalanced or a balanced status. [review]
Studies strongly implicates RANK and RANKL as key molecules involved in the initiation of BRCA1-associated breast cancer. [review]
RANK is frequently expressed by cancer cells in contrast with RANKL (show TNFSF11 Antibodies) which is frequently detected in the tumor microenvironment, and together they participate in every step in cancer development. (Review)
EGFR (show EGFR Antibodies) and RANK combinatorial in vitro analyses revealed a significant upregulation of AKT (show AKT1 Antibodies) and ERK (show EPHB2 Antibodies) signaling after EGF (show EGF Antibodies) stimulation in cell lines and also an increase of breast cancer cell invasiveness.
RANK/RANKL (show TNFSF11 Antibodies) signaling is involved in the androgen deprivation therapy-induced acceleration of bone metastasis in castration-insensitive prostate cancer and is inhibited by osteoprotegerin (show TNFRSF11B Antibodies) to prevent bone metastasis.
In histologically normal tissue of BRCA1-mutation carriers and showed that RANK(+) cells are highly proliferative, have grossly aberrant DNA repair and bear a molecular signature similar to that of basal-like breast cancer.
The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptors can interact with various TRAF family proteins, through which this receptor induces the activation of NF-kappa B and MAPK8/JNK. This receptor and its ligand are important regulators of the interaction between T cells and dendritic cells. This receptor is also an essential mediator for osteoclast and lymph node development. Mutations at this locus have been associated with familial expansile osteolysis, autosomal recessive osteopetrosis, and Paget disease of bone. Alternatively spliced transcript variants have been described for this locus.
tumor necrosis factor receptor superfamily member 11A
, tumor necrosis factor receptor superfamily, member 11a, NFKB activator
, receptor activator of nuclear factor-kappa B
, tumor necrosis factor receptor superfamily member 11A-like
, osteoclast differentiation factor receptor
, receptor activator of NF-KB
, receptor activator of NF-kappaB
, loss of heterozygosity, 18, chromosomal region 1