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anti-Human TNFSF11 Antibodies:
anti-Mouse (Murine) 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 20 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 10 Pubmed References
Human Monoclonal TNFSF11 Primary Antibody for ELISA - ABIN4249074
Pearse, Sordillo, Yaccoby, Wong, Liau, Colman, Michaeli, Epstein, Choi: Multiple myeloma disrupts the TRANCE/ osteoprotegerin cytokine axis to trigger bone destruction and promote tumor progression. in Proceedings of the National Academy of Sciences of the United States of America 2001
Show all 9 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
Show all 4 Pubmed References
Human Monoclonal TNFSF11 Primary Antibody for CyTOF, FACS - ABIN4361916
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 FACS, IHC (fro) - ABIN252684
Shetty, Pepin, Charest, Perron, Doyle, Voisine, Dagenais, Pibarot, Mathieu: Expression of bone-regulatory proteins in human valve allografts. in Heart (British Cardiac Society) 2006
Show all 3 Pubmed References
Human Polyclonal TNFSF11 Primary Antibody for IHC, IHC (p) - ABIN4361905
Lim, Liu, Hunter, Cheng, Mah, Helms: Downregulation of Wnt causes root resorption. in American journal of orthodontics and dentofacial orthopedics : official publication of the American Association of Orthodontists, its constituent societies, and the American Board of Orthodontics 2014
Show all 2 Pubmed References
Higher concentrations of serum sRANKL were positively associated with risk of estrogen receptor (show ESR1 Antibodies) positive breast cancer.
RANKL is overexpressed in invariant NKT (show SLC22A6 Antibodies) cells in bone marrow of patients with multiple myeloma.
triple-negative breast cancer (TNBC) patients that expressed both RANK and RANKL proteins had significantly worse RFS and OS than patients with RANK-positive, RANKL-negative tumors. RANKL was an independent, poor prognostic factor for RFS and OS in multivariate analysis in samples that expressed both RANK and RANKL.
Findings suggest that cell-autonomous activation of the RANKL/RANK signaling axis is a convergently shared, non-oncogenic addiction underlying the generation and maintenance of CSC-like states in response to diverse molecular events such as BRCA1 haploinsufficiency and EMT (show ITK Antibodies) phenomena.
Data suggest that, in children with type I diabetes, serum levels of osteoprotegerin (show TNFRSF11B Antibodies) are up-regulated, serum levels of RANKL are unchanged, and serum levels of fetuin-A (show AHSG Antibodies) are down-regulated. (RANKL = receptor activator of nuclear factor kappa B ligand)
There was no significant difference in GCF (show GUCY2F Antibodies) RANKL values among groups (P > 0.05) or during the observation period (P > 0.008). The use of BP may be effective in preventing periodontal breakdown by controlling the levels of these markers in osteoporosis as an adjunct to periodontal treatment
Data report that in postmenopausal women without known genetic predisposition, high RANKL serum levels stratify a subpopulation of women at high risk of developing breast cancer 12-24 months before diagnosis.
Data suggest that STAT6 (show STAT6 Antibodies) and RANKL are involved in regulation of apoptosis, gene expression, and cell proliferation in hepatocellular carcinoma cell lines; depletion of STAT6 (show STAT6 Antibodies) using RNA interference increases apoptosis; this mechanism involves down-regulation of expression of RANKL. (STAT6 (show STAT6 Antibodies) = signal transducer and activator of transcription 6 (show STAT6 Antibodies); RANKL = receptor activator of nuclear factor kappa B ligand)
Positivity of RANKL and anti-CCP2 (show AGBL2 Antibodies) yielded significant risk for progression with negativity for both as reference. No single nucleotide polymorphism encoding TNFSF11 or SOST (show SOST Antibodies) was associated with increased concentrations of the factors.
The compound with greatest potential is E05657 with high activity and low effective concentration in the HTS (show APCDD1 Antibodies) system. It increases the OPG/RANKL ratio and OPG (show TNFRSF11B Antibodies) secretion, decreases the NFATc1 (show NFATC1 Antibodies) expression, and reduces osteoclastogenesis in vitro
LPS (show TLR4 Antibodies) increased mRNA and protein expressions of IL-6 (show IL6 Antibodies) 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 (show STAT5A Antibodies) contributes to the remarkable IL-3 (show IL-3 Antibodies)-mediated inhibition of RANKL-induced osteoclastogenesis by activating Id genes and their associated pathways.
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.
These results suggest that LOX (show LOX Antibodies) has the ability to induce RANKL expression on stromal cells; however, it fails to substitute for RANKL in osteoclastogenesis.
Results demonstrated picroside II strongly inhibited RANKL-induced osteoclast formation when added during the early stage of BMMs cultures, suggesting that it acts on osteoclast precursors to inhibit RANKL/RANK signaling.
loss of BMP signaling specifically in osteocytes dramatically increases bone mass presumably through simultaneous inhibition of RANKL and SOST (show SOST Antibodies), leading to osteoclast inhibition and Wnt (show WNT2 Antibodies) activation together.
The potentiation of RANKL induced CTX release by dexamethasone was significantly less in bone marrow macrophage cells from mice with conditional knockout of the osteoclastic glucocorticoid receptor (show NR3C1 Antibodies) and completely absent in cells from GR(dim) mice, which carry a point mutation in one dimerizing interface of the GC receptor.
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