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TNFalpha and RANKL promote osteoclastogenesis by upregulating RANK via the NFkappaB pathway.
Results from this study demonstrate that RANK signalling in NPY (show NPY Proteins) neurons is involved in modulating NPY (show NPY Proteins) levels and through that matching bone mass to body weight.
the investigation of RANK and RANKL (show TNFSF11 Proteins) as possible novel immunotherapy targets in cancer is a rational approach. Here we have defined the mechanism of action of RANKL (show TNFSF11 Proteins)-RANK blockade in combination with anti-CTLA4 (show CTLA4 Proteins), 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 (show EPHB2 Proteins)/Mitf (show MITF Proteins) signalling. In addition, the results suggest that baicalin can potentially be used as a natural product for the treatment of bone fracture
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.
study identified the second disease gene for DOS. TNFRSF11A (show TNFRSF11A Proteins) isoforms may have the different roles in skeletal development and metabolism
The mRNA expression of RANK was highest in prostate tumour tissue from patients with bone metastases as compared to BPH or locally confined tumours, also shown in clinical subgroups distinguished by Gleason Score or PSA level.
For the RANK gene, the AGTGC haplotype was associated with the lowest risk of presenting chronic joint pain in individuals without TMD (show TTN Proteins) (P=0.03). This study supports the hypothesis that changes in the OPG (show TNFRSF11B Proteins) and RANK genes influence the presence of chronic joint pain in individuals with and without TMD (show TTN Proteins).
In this study, whole exome sequencing (WES) was successfully used in six patients with malignant infantile osteopetrosis (show CSF1 Proteins) (MIOP) and identified mutations in four MIOP-related genes (CLCN7 (show CLCN7 Proteins), TCIRG1 (show TCIRG1 Proteins), SNX10 (show SNX10 Proteins), and TNFRSF11A (show TNFRSF11A Proteins)).
triple-negative breast cancer (TNBC) patients that expressed both RANK and RANKL (show TNFSF11 Proteins) proteins had significantly worse RFS and OS than patients with RANK-positive, RANKL (show TNFSF11 Proteins)-negative tumors. RANKL (show TNFSF11 Proteins) was an independent, poor prognostic factor for RFS and OS in multivariate analysis in samples that expressed both RANK and RANKL (show TNFSF11 Proteins).
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.
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