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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
High RANKL expression is associated with gastric cancer cell migration.
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 (show GLI3 Proteins) tissue but did not exceed as much as in the tumour tissue.
In cardiovascular risks, OPG (show TNFRSF11B Proteins) 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 (show CYP11A1 Proteins) patients.
sRANKL and OPG (show TNFRSF11B Proteins) may play a role in the pathogenesis of diabetes as well as metabolic disturbance
regulation of OSCAR by TNF-alpha (show TNF Proteins) 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 (show MLXIP Proteins)-217 is a useful diagnostic biomarker and is involved in human podocyte cells apoptosis via targeting TNFSF11 in membranous nephropathy.
Vascular smooth cells are a significant source of osteoprotegerin (show TNFRSF11B Proteins) within the vasculature but that RANKL, once present, downregulates this production and appears capable of preventing the "protective" upregulation of OPG (show TNFRSF11B Proteins) seen with VSMCs exposed to physiological levels of cyclic strain.
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 (show CTLA4 Proteins), 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 (show FOXO1 Proteins) transcriptional activity by inhibiting the PI3K/AKT (show AKT1 Proteins) signaling pathway, and hence promoted resistance to oxidative damage and restrained osteoclastogenesis. Inhibition of the PI3K/AKT (show AKT1 Proteins) 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 (show ADORA2B Proteins) stimulation inhibits the activation of ERK1/2, p38 (show CRK Proteins) and NF-kappaB (show NFKB1 Proteins) 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 (show ITGAM Proteins) promotes the differentiation of osteoclasts induced by RANKL through the Syk (show SYK Proteins) signaling pathway.
RANKL and Src (show SRC Proteins) has an unrecognized role in osteocyte survival.
compressive force induced the differentiation of RAW264.7 from increase in RANK and decrease in LGR4 (show LGR4 Proteins) expression.
miR (show MLXIP Proteins)-145 expression was inhibited in RANKL-induced osteoclastogenesis
LPS (show TLR4 Proteins) increased mRNA and protein expressions of IL-6 (show IL6 Proteins) and RANKL on day 14
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