Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
RANKL (show TNFSF11 Proteins)/RANK control progenitor cell expansion and tumorigenesis in inherited breast cancer.
Artesunate inhibits RANKL (show TNFSF11 Proteins)-induced osteoclastogenesis by suppressing the NF-kappaB (show NFKB1 Proteins) signaling pathway.
Data suggest that mutations at position I248 in DE-loop of murine RANKL (show TNFSF11 Proteins) have effects on interaction of RANKL (show TNFSF11 Proteins) with RANK and on subsequent activation of osteoclastogenesis by this hetero-multimer. (RANKL (show TNFSF11 Proteins) = osteoclast differentiation factor (show TNFSF11 Proteins); RANK = tumor necrosis factor (show TNF Proteins) receptor superfamily, member 11a protein)
The persistence of bone erosion and synovial osteoclasts in Rank-deficient mice, and the ability of TNF (show TNF Proteins)/IL-6 (show IL6 Proteins) 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 Proteins)+)storage and SERCA (show ATP2A3 Proteins) activity, ultimately affecting denervated skeletal muscle function.
present study shows that ginsenoside Rg3 protects against LPS (show TLR4 Proteins)-induced acute lung injury through inactivating the NF-kappaB (show NFKB1 Proteins) signaling
In palmatine-treated mice, RANKL (show TNFSF11 Proteins) and OPG (show TNFSF11 Proteins) expression decreased. In the culture supernatant of MC3T3-E1 cells, RANKL (show TNFSF11 Proteins) and OPG (show TNFSF11 Proteins) 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 Proteins)/RANK affinity and osteoclastogenic capacity.
Dissection of the mechanism by which this occurs indicates that mCripto-1 activates receptor activator NF-kappaB (show NFKB1 Proteins)/receptor activator NF-kappaB (show NFKB1 Proteins) ligand, and NF-kappaB (show NFKB1 Proteins) signaling pathways.
We also show that R-spondin1 (show RSPO1 Proteins) is depleted in RANK-null progenitors, and that its exogenous administration rescues key aspects of RANK deficiency by reinstating a WNT (show WNT2 Proteins) response and mammary cell expansion
RANK is increased in hormone receptor (show NR4A1 Proteins) 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 Proteins)/RANK system function, and the pulsatility and circadian rhythmicity of these hormones may induce an oscillatory fluctuation of the OPG/ RANKL (show TNFSF11 Proteins) ratio. Also, psycological characteristics may provoke a shift of the OPG/ RANKL (show TNFSF11 Proteins) 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 Proteins) which is frequently detected in the tumor microenvironment, and together they participate in every step in cancer development. (Review)
EGFR (show EGFR Proteins) and RANK combinatorial in vitro analyses revealed a significant upregulation of AKT (show AKT1 Proteins) and ERK (show EPHB2 Proteins) signaling after EGF (show EGF Proteins) stimulation in cell lines and also an increase of breast cancer cell invasiveness.
RANK/RANKL (show TNFSF11 Proteins) 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 Proteins) 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 Proteins) 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 Proteins), RANK, and OPG (show TNFRSF11B Proteins) 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 Proteins) is a novel TRAF6 (show TRAF6 Proteins) interaction partner that functions in the activation of cooperative signaling between T6BSs and the IVVY motif in the RANK signaling complex.
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.
osteoclast differentiation factor receptor
, receptor activator of NF-KB
, receptor activator of NF-kappaB
, tumor necrosis factor receptor superfamily member 11A
, loss of heterozygosity, 18, chromosomal region 1
, receptor activator of nuclear factor-kappa B