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Artesunate inhibits RANKL (show TNFSF11 ELISA Kits)-induced osteoclastogenesis by suppressing the NF-kappaB (show NFKB1 ELISA Kits) signaling pathway.
Data suggest that mutations at position I248 in DE-loop of murine RANKL (show TNFSF11 ELISA Kits) have effects on interaction of RANKL (show TNFSF11 ELISA Kits) with RANK and on subsequent activation of osteoclastogenesis by this hetero-multimer. (RANKL (show TNFSF11 ELISA Kits) = osteoclast differentiation factor (show TNFSF11 ELISA Kits); RANK = tumor necrosis factor (show TNF ELISA Kits) receptor superfamily, member 11a protein)
The persistence of bone erosion and synovial osteoclasts in Rank-deficient mice, and the ability of TNF (show TNF ELISA Kits)/IL-6 (show IL6 ELISA Kits) 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 ELISA Kits)+)storage and SERCA (show ATP2A3 ELISA Kits) activity, ultimately affecting denervated skeletal muscle function.
present study shows that ginsenoside Rg3 protects against LPS (show TLR4 ELISA Kits)-induced acute lung injury through inactivating the NF-kappaB (show NFKB1 ELISA Kits) signaling
In palmatine-treated mice, RANKL (show TNFSF11 ELISA Kits) and OPG (show TNFSF11 ELISA Kits) expression decreased. In the culture supernatant of MC3T3-E1 cells, RANKL (show TNFSF11 ELISA Kits) and OPG (show TNFSF11 ELISA Kits) 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 ELISA Kits)/RANK affinity and osteoclastogenic capacity.
Dissection of the mechanism by which this occurs indicates that mCripto-1 activates receptor activator NF-kappaB (show NFKB1 ELISA Kits)/receptor activator NF-kappaB (show NFKB1 ELISA Kits) ligand, and NF-kappaB (show NFKB1 ELISA Kits) signaling pathways.
We also show that R-spondin1 (show RSPO1 ELISA Kits) is depleted in RANK-null progenitors, and that its exogenous administration rescues key aspects of RANK deficiency by reinstating a WNT (show WNT2 ELISA Kits) response and mammary cell expansion
findings have uncovered a tumorigenic role for RANKL (show TNFSF11 ELISA Kits)/RANK in the salivary gland and suggest that targeting this pathway may represent a novel therapeutic intervention approach in the prevention and/or treatment of this understudied head and neck cancer
Studies showed that the central hypothalamic-pituitary regulatory system, via it's relative hormones, seems to control OPG/RANKL (show TNFSF11 ELISA Kits)/RANK system function, and the pulsatility and circadian rhythmicity of these hormones may induce an oscillatory fluctuation of the OPG/ RANKL (show TNFSF11 ELISA Kits) ratio. Also, psycological characteristics may provoke a shift of the OPG/ RANKL (show TNFSF11 ELISA Kits) 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 ELISA Kits) which is frequently detected in the tumor microenvironment, and together they participate in every step in cancer development. (Review)
EGFR (show EGFR ELISA Kits) and RANK combinatorial in vitro analyses revealed a significant upregulation of AKT (show AKT1 ELISA Kits) and ERK (show EPHB2 ELISA Kits) signaling after EGF (show EGF ELISA Kits) stimulation in cell lines and also an increase of breast cancer cell invasiveness.
RANK/RANKL (show TNFSF11 ELISA Kits) 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 ELISA Kits) 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.
In this review, we will provide a summary of the biological functions of RANK signaling pathway (receptor activator of nuclear factor kappaB ligand RANKL (show TNFSF11 ELISA Kits) and its receptor RANK ) and downstream pathways in bone remodeling, immunity and epithelial homeostasis, with a particular emphasis on cancer
Our results suggest that the polymorphism of the RANKL (show TNFSF11 ELISA Kits), RANK, and OPG (show TNFRSF11B ELISA Kits) genes does not make a significant genetic contribution to heel ultrasound measurements in a population of young Caucasian adults. Further studies replicating the results in independent populations are needed to support these initial findings.
Vav3 (show VAV3 ELISA Kits) is a novel TRAF6 (show TRAF6 ELISA Kits) interaction partner that functions in the activation of cooperative signaling between T6BSs and the IVVY motif in the RANK signaling complex.
OPG (show TNFRSF11B ELISA Kits) rs2073618, RANK rs75404003, and RANKL (show TNFSF11 ELISA Kits) rs9594782 single nucleotide poymorphisms may predispose LVH in thalassemia patients.
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