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results reveal a novel ERRalpha/RANK axis by which ERRalpha in primary breast cancer promotes early dissemination of cancer cells to bone. These findings suggest that ERRalpha may be a useful therapeutic target to prevent bone metastases.
Additional protein interaction characterization revealed epidermal growth factor receptor (EGFR) as a novel interacting partner for RANK-c in breast cancer cells.
lactation increases physiological maxillary bone remodeling and orthodontic tooth movement, and both require activation of RANK/RANKL/OPG system
RANK deficiency ameliorates podocyte injury by suppressing calcium/calcineurin/NFATc1 signaling
TNFalpha and RANKL promote osteoclastogenesis by upregulating RANK via the NFkappaB pathway.
Results from this study demonstrate that RANK signalling in NPY neurons is involved in modulating NPY levels and through that matching bone mass to body weight.
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, 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/Mitf signalling. In addition, the results suggest that baicalin can potentially be used as a natural product for the treatment of bone fracture
RANKL/RANK control progenitor cell expansion and tumorigenesis in inherited breast cancer.
RANK rewires energy homeostasis in murine lung cancer cells and promotes expansion of lung cancer stem-like cells
Artesunate inhibits RANKL-induced osteoclastogenesis by suppressing the NF-kappaB signaling pathway.
Data suggest that mutations at position I248 in DE-loop of murine RANKL have effects on interaction of RANKL with RANK and on subsequent activation of osteoclastogenesis by this hetero-multimer. (RANKL = osteoclast differentiation factor; RANK = tumor necrosis factor receptor superfamily, member 11a protein)
The persistence of bone erosion and synovial osteoclasts in Rank-deficient mice, and the ability of TNF/IL-6 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+)storage and SERCA activity, ultimately affecting denervated skeletal muscle function.
present study shows that ginsenoside Rg3 protects against LPS-induced acute lung injury through inactivating the NF-kappaB signaling
In palmatine-treated mice, RANKL and OPG expression decreased. In the culture supernatant of MC3T3-E1 cells, RANKL and OPG 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/RANK affinity and osteoclastogenic capacity.
Dissection of the mechanism by which this occurs indicates that mCripto-1 activates receptor activator NF-kappaB/receptor activator NF-kappaB ligand, and NF-kappaB signaling pathways.
We also show that R-spondin1 is depleted in RANK-null progenitors, and that its exogenous administration rescues key aspects of RANK deficiency by reinstating a WNT response and mammary cell expansion
KLF5 and TNFRSF11a are related to cervical cancer. KLF5 promotes the proliferation, migration, and invasion of cervical cancer cells partly by upregulating the transcription of TNFRSF11a.
Changes in cerebrospinal fluid levels of the RANKL/RANK/OPG axis are associated with multiple sclerosis, particularly at disease onset.
RANK/RANKL were identified as crucial regulators for BRCA1 mutation-driven breast cancer. Current prevention strategies for BRCA1 mutation carriers are associated with wide-ranging risks; therefore, the search for alternative, non-invasive strategies is of paramount importance
Reduced miR-144-3p expression in serum and bone mediates osteoporosis pathogenesis by targeting RANK.
findings indicate that C/EBPalpha is a stronger inducer of osteoclast differentiation than c-Fos, partly via C/EBPalpha regulation by the RANK (535)IVVY(538) motif
gammadelta T cells suppressed iDCs osteoclastogenesis by downregulation of the RANK/cFos/ATP6V0D2 signaling pathway.
RANK protein expression increased from normal to malignant endometrium, and the expression level was related with tumor grade but not with stage or the age of subjects in endometrial cancer.
study identified the second disease gene for DOS. TNFRSF11A 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.
RANK 575C>T polymorphisms did not show any statistically significant differences between the study groups (Osteoporosis and Osteopenia) and Postmenopausal women.
For the RANK gene, the AGTGC haplotype was associated with the lowest risk of presenting chronic joint pain in individuals without TMD (P=0.03). This study supports the hypothesis that changes in the OPG and RANK genes influence the presence of chronic joint pain in individuals with and without TMD.
In this study, whole exome sequencing (WES) was successfully used in six patients with malignant infantile osteopetrosis (MIOP) and identified mutations in four MIOP-related genes (CLCN7, TCIRG1, SNX10, and TNFRSF11A).
triple-negative breast cancer (TNBC) patients that expressed both RANK and RANKL proteins had significantly worse RFS and OS than patients with RANK-positive, RANKL-negative tumors. RANKL was an independent, poor prognostic factor for RFS and OS in multivariate analysis in samples that expressed both RANK and RANKL.
RANK is increased in hormone receptor negative and basal breast cancer, and correlates with worse recurrence-free survival and risk of bone metastasis.
RANK SNP rs34945627 has a high allelic frequency in patients with breast cancer and Bone metastases, and is associated with decreased disease-free survival and Overall Survival.
RANK rewires energy homeostasis in human lung cancer cells and promotes expansion of lung cancer stem-like cells.
Studies showed that the central hypothalamic-pituitary regulatory system, via it's relative hormones, seems to control OPG/RANKL/RANK system function, and the pulsatility and circadian rhythmicity of these hormones may induce an oscillatory fluctuation of the OPG/ RANKL ratio. Also, psycological characteristics may provoke a shift of the OPG/ RANKL 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 which is frequently detected in the tumor microenvironment, and together they participate in every step in cancer development. (Review)
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