Browse our TNFRSF11A Proteins (TNFRSF11A)

Mouse (Murine) Tumor Necrosis Factor Receptor Superfamily, Member 11a, NFKB Activator (TNFRSF11A) interaction partners

1. Insulin induces RANK expression via ERK1/2, which contributes to the enhancement of osteoclast differentiation.

2. 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

3. RANKL (show TNFSF11 Proteins)/RANK control progenitor cell expansion and tumorigenesis in inherited breast cancer.

4. Artesunate inhibits RANKL (show TNFSF11 Proteins)-induced osteoclastogenesis by suppressing the NF-kappaB (show NFKB1 Proteins) signaling pathway.

5. 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)

6. 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.

7. 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.

8. 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

9. 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.

10. 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.

Human Tumor Necrosis Factor Receptor Superfamily, Member 11a, NFKB Activator (TNFRSF11A) interaction partners

1. 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).

2. 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).

3. 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.

4. 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]

5. Studies strongly implicates RANK and RANKL as key molecules involved in the initiation of BRCA1-associated breast cancer. [review]

6. 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)

7. 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.

8. 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.

9. 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.

10. 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