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the investigation of RANK and RANKL (zeige TNFSF11 Proteine) as possible novel immunotherapy targets in cancer is a rational approach. Here we have defined the mechanism of action of RANKL (zeige TNFSF11 Proteine)-RANK blockade in combination with anti-CTLA4 (zeige CTLA4 Proteine), and provide insight into the combination efficacy observed in the case reports.
Insulin induces RANK expression via ERK1/2, which contributes to the enhancement of osteoclast differentiation.
This indicated that RANK might be the binding target of baicalin. In sum, our findings revealed baicalin increased osteoclast maturation and function via p-ERK (zeige EPHB2 Proteine)/Mitf (zeige MITF Proteine) signalling. In addition, the results suggest that baicalin can potentially be used as a natural product for the treatment of bone fracture
RANKL (zeige TNFSF11 Proteine)/RANK control progenitor cell expansion and tumorigenesis in inherited breast cancer.
Artesunate inhibits RANKL (zeige TNFSF11 Proteine)-induced osteoclastogenesis by suppressing the NF-kappaB (zeige NFKB1 Proteine) signaling pathway.
Data suggest that mutations at position I248 in DE-loop of murine RANKL (zeige TNFSF11 Proteine) have effects on interaction of RANKL (zeige TNFSF11 Proteine) with RANK and on subsequent activation of osteoclastogenesis by this hetero-multimer. (RANKL (zeige TNFSF11 Proteine) = osteoclast differentiation factor (zeige TNFSF11 Proteine); RANK = tumor necrosis factor (zeige TNF Proteine) receptor superfamily, member 11a protein)
The persistence of bone erosion and synovial osteoclasts in Rank-deficient mice, and the ability of TNF (zeige TNF Proteine)/IL-6 (zeige IL6 Proteine) 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 (zeige CA2 Proteine)+)storage and SERCA (zeige ATP2A3 Proteine) activity, ultimately affecting denervated skeletal muscle function.
present study shows that ginsenoside Rg3 protects against LPS (zeige TLR4 Proteine)-induced acute lung injury through inactivating the NF-kappaB (zeige NFKB1 Proteine) signaling
In palmatine-treated mice, RANKL (zeige TNFSF11 Proteine) and OPG (zeige TNFSF11 Proteine) expression decreased. In the culture supernatant of MC3T3-E1 cells, RANKL (zeige TNFSF11 Proteine) and OPG (zeige TNFSF11 Proteine) levels were significantly reduced by palmatine addition.
For the RANK gene, the AGTGC haplotype was associated with the lowest risk of presenting chronic joint pain in individuals without TMD (zeige TTN Proteine) (P=0.03). This study supports the hypothesis that changes in the OPG (zeige TNFRSF11B Proteine) and RANK genes influence the presence of chronic joint pain in individuals with and without TMD (zeige TTN Proteine).
In this study, whole exome sequencing (WES) was successfully used in six patients with malignant infantile osteopetrosis (zeige CSF1 Proteine) (MIOP) and identified mutations in four MIOP-related genes (CLCN7 (zeige CLCN7 Proteine), TCIRG1 (zeige TCIRG1 Proteine), SNX10 (zeige SNX10 Proteine), and TNFRSF11A).
triple-negative breast cancer (TNBC) patients that expressed both RANK and RANKL (zeige TNFSF11 Proteine) proteins had significantly worse RFS and OS than patients with RANK-positive, RANKL (zeige TNFSF11 Proteine)-negative tumors. RANKL (zeige TNFSF11 Proteine) was an independent, poor prognostic factor for RFS and OS in multivariate analysis in samples that expressed both RANK and RANKL (zeige TNFSF11 Proteine).
RANK is increased in hormone receptor (zeige NR4A1 Proteine) 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 (zeige TNFSF11 Proteine)/RANK system function, and the pulsatility and circadian rhythmicity of these hormones may induce an oscillatory fluctuation of the OPG/ RANKL (zeige TNFSF11 Proteine) ratio. Also, psycological characteristics may provoke a shift of the OPG/ RANKL (zeige TNFSF11 Proteine) 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 (zeige TNFSF11 Proteine) which is frequently detected in the tumor microenvironment, and together they participate in every step in cancer development. (Review)
EGFR (zeige EGFR Proteine) and RANK combinatorial in vitro analyses revealed a significant upregulation of AKT (zeige AKT1 Proteine) and ERK (zeige EPHB2 Proteine) signaling after EGF (zeige EGF Proteine) stimulation in cell lines and also an increase of breast cancer cell invasiveness.
RANK/RANKL (zeige TNFSF11 Proteine) signaling is involved in the androgen deprivation therapy-induced acceleration of bone metastasis in castration-insensitive prostate cancer and is inhibited by osteoprotegerin (zeige TNFRSF11B Proteine) 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.
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