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Mouse (Murine) TNFSF11 Protein expressed in HEK-293 Cells - ABIN1344301
Beleut, Rajaram, Caikovski, Ayyanan, Germano, Choi, Schneider, Brisken: Two distinct mechanisms underlie progesterone-induced proliferation in the mammary gland. in Proceedings of the National Academy of Sciences of the United States of America 2010
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 Proteins) phenomena.
Data suggest that, in children with type I diabetes, serum levels of osteoprotegerin (show TNFRSF11B Proteins) are up-regulated, serum levels of RANKL are unchanged, and serum levels of fetuin-A (show AHSG Proteins) are down-regulated. (RANKL = receptor activator of nuclear factor kappa B ligand)
There was no significant difference in GCF (show GUCY2F Proteins) 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 Proteins) and RANKL are involved in regulation of apoptosis, gene expression, and cell proliferation in hepatocellular carcinoma cell lines; depletion of STAT6 (show STAT6 Proteins) using RNA interference increases apoptosis; this mechanism involves down-regulation of expression of RANKL. (STAT6 (show STAT6 Proteins) = signal transducer and activator of transcription 6 (show STAT6 Proteins); RANKL = receptor activator of nuclear factor kappa B ligand)
Positivity of RANKL and anti-CCP2 yielded significant risk for progression with negativity for both as reference. No single nucleotide polymorphism encoding TNFSF11 or SOST (show SOST Proteins) 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 Proteins) system. It increases the OPG/RANKL ratio and OPG (show TNFRSF11B Proteins) secretion, decreases the NFATc1 (show NFATC1 Proteins) expression, and reduces osteoclastogenesis in vitro
Our study suggests that the RANKL/RANK pathway contributes to the development and maintenance of the immunosuppressive tumor microenvironment and denosumab may be a promising adjuvant therapy targeting TAMs in cancer of apocrine origin
RANKL/Osteoprotegerin (show TNFRSF11B Proteins) have roles in bone turnover in Hashimoto Thyroiditis
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 Proteins) 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 Proteins), leading to osteoclast inhibition and Wnt (show WNT2 Proteins) 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 Proteins) and completely absent in cells from GR(dim) mice, which carry a point mutation in one dimerizing interface of the GC receptor.
findings demonstrate that mTORC1 activation-stimulated RANKL expression in B cells is sufficient to induce bone loss and osteoporosis. The study also established a link between mTORC1 and the RANKL/OPG axis via negative regulation of beta-catenin (show CTNNB1 Proteins).
dihydroartemisinin inhibited RANKL-induced NF-kappaB (show NFKB1 Proteins) and NFAT (show NFATC1 Proteins) activity.
Cyanidin chloride is capable of inhibiting osteoclast formation, hydroxyapatite resorption and RANKL-induced signal pathways in vitro and ovariectomy-induced bone loss in vivo.
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
, osteoclastogenesis inhibitory factor
, tumor necrosis factor receptor superfamily member 11B
, 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