Recombinant Mouse Tumor necrosis factor ligand superfamily member 11(Tnfsf11),partial

1. The results demonstrate that the membrane-bound form of RANKL is sufficient for most functions of this protein but that the soluble form does contribute to physiological bone remodeling in adult mice. PMID: 30046091
2. the molecular level, we confirmed, for the first time, that RES upregulated FoxO1 transcriptional activity by inhibiting the PI3K/AKT signaling pathway, and hence promoted resistance to oxidative damage and restrained osteoclastogenesis. Inhibition of the PI3K/AKT signaling pathway may be induced by RANKL. PMID: 29115382
3. Deletion of the RANKL D5 enhancer delays the progression of atherosclerotic plaque development and plaque calcification in hypercholesterolemic mice. PMID: 28419519
4. these results suggest that A2BAR stimulation inhibits the activation of ERK1/2, p38 and NF-kappaB by RANKL, which suppresses the induction of osteoclast marker genes, thus contributing to the decrease in osteoclast cell-cell fusion and bone resorption activity. PMID: 29047264
5. compressive force induced the differentiation of RAW264.7 from increase in RANK and decrease in LGR4 expression. PMID: 29572179
6. miR-145 expression was inhibited in RANKL-induced osteoclastogenesis PMID: 29577879
7. LPS increased mRNA and protein expressions of IL-6 and RANKL on day 14 PMID: 28637991
8. hBD-1 potentiates the induction of in vitro osteoclastogenesis by RANKL via enhanced phosphorylation of the p44/42 MAPKs PMID: 28709835
9. In conclusion, the results suggest that linarin has anti-osteoclastic effects and may serve as potential modulatory agents for the prevention and treatment of bone loss-associated diseases. PMID: 29269297
10. Rankl(-/-) bone marrow-mesenchymal stromal cell displayed reduced clonogenicity and osteogenic capacity. PMID: 28100034
11. In this study, the authors identified by gene expression profiling that microgravity induces high levels of TRAIL expression in murine preosteoclast cells in the absence of RANKL stimulation compared to ground based cultures. PMID: 27142480
12. These results suggest that LOX has the ability to induce RANKL expression on stromal cells; however, it fails to substitute for RANKL in osteoclastogenesis. PMID: 27606829
13. Results demonstrated picroside II strongly inhibited RANKL-induced osteoclast formation when added during the early stage of BMMs cultures, suggesting that it acts on osteoclast precursors to inhibit RANKL/RANK signaling. PMID: 28464271
14. loss of BMP signaling specifically in osteocytes dramatically increases bone mass presumably through simultaneous inhibition of RANKL and SOST, leading to osteoclast inhibition and Wnt activation together. PMID: 27402532
15. The potentiation of RANKL induced CTX release by dexamethasone was significantly less in bone marrow macrophage cells from mice with conditional knockout of the osteoclastic glucocorticoid receptor and completely absent in cells from GR(dim) mice, which carry a point mutation in one dimerizing interface of the GC receptor. PMID: 27596806
16. findings demonstrate that mTORC1 activation-stimulated RANKL expression in B cells is sufficient to induce bone loss and osteoporosis. The study also established a link between mTORC1 and the RANKL/OPG axis via negative regulation of beta-catenin. PMID: 26825871
17. dihydroartemisinin inhibited RANKL-induced NF-kappaB and NFAT activity. PMID: 26684711
18. Cyanidin chloride is capable of inhibiting osteoclast formation, hydroxyapatite resorption and RANKL-induced signal pathways in vitro and ovariectomy-induced bone loss in vivo. PMID: 28771720
19. Together these data indicate that osteocyte apoptosis plays a central and controlling role in triggering osteocyte RANKL production and the activation of new resorption leading to bone loss in disuse. PMID: 26852281
20. data suggest that, particularly with combination treatment of zoledronic acid (ZA) and glucocorticoids, surviving lymphocytes might be the source of inflammation-induced sRANKL. Thus, circulating sRANKL levels might be modulated by ZA. PMID: 26999703
21. matrine abrogated RANKL-induced activation of NF-kappaB, AKT, and MAPK pathways and suppressed osteoclastogenesis-related marker expression, including matrix metalloproteinase 9, NFATc1, TRAP, C-Src, and cathepsin K PMID: 28739641
22. The anti-osteoclastic and anti-resorptive actions of Luteoloside are mediated via blocking NFATc1 activity and the attenuation of RANKL-mediated Ca(2+) signaling as well as NF-kappaB and MAPK pathways. PMID: 28681916
23. Osteoprotegerin facilitates pulmonary arterial hypertension pathogenesis by regulating pulmonary arterial smooth muscle cell proliferation via integrin alphavbeta3/FAK/AKT signaling pathway. PMID: 28077433
24. results demonstrate that IL-15 and RANKL induce osteoclastogenesis synergistically, and IL-15 might play a novel and major role in destructive inflammatory bone diseases PMID: 27608420
25. Absence of Musashi2 in osteoclast precursors promotes apoptosis and inhibits RANKL-induced NF-kappaB activation, which is essential for osteoclast survival. PMID: 27441652
26. This study demonstrates that Col6a1-Cre driver mice are as useful as Twist2-Cre driver mice for functional analyses of GALT-resident mesenchymal cells, including MCi cells. PMID: 28882590
27. Estrogens and androgens inhibit osteoblast-driven osteoclastogenesis through non-genomic mechanism(s) that entail, MMP-mediated RANKL dissociation from the cell membrane. PMID: 28213978
28. sRANKL increased macrophage glucose uptake at normal glucose concentrations, which was impaired by hyperglycemia pretreatment through the inhibition of Glut1 membrane translocation and the insulin receptor and IRS-1 gene transcription. PMID: 28624040
29. Our findings show that anti-RANKL antibody administration during pregnancy results in not only an undesirable increase in bone mass, but also has harmful effects on newborn survival. PMID: 28760341
30. RANKL represses the transcription of the E3 ubiquitin ligase RNF146 through an NF-kappaB-related inhibitory element in the RNF146 promoter. PMID: 28287403
31. This study showed that RANKL favors osteoclastogenesis via attenuation of Nrf2-mediated antioxidant enzyme expression by competing with Bach1 nuclear accumulation. PMID: 27836987
32. Membrane-bound RANKL induces M cell differentiation and CCL20 expression in the follicle associated epithelium of gut-associated lymphoid tissues. PMID: 28436956
33. The data show that S. aureus enhances bone resorption and periosteal osteoclast formation by increasing osteoblast RANKL production through TLR2. PMID: 27311019
34. Data (including data from studies using knockout mice) suggest that RANKL enhances TNF-induced osteoclast formation from precursor spleen cells and enhances bone resorption independently of Traf6 by degrading Traf3, a known inhibitor of osteoclastogenesis. (RANKL = osteoclast differentiation factor; TNF = tumor necrosis factor; Traf = TNF receptor-associated factor) PMID: 28438834
35. Results suggest that MAPK signaling pathway is necessary for receptor activator of nuclear factor kappa-B ligand (RANKL) expression in bone marrow stromal cell. PMID: 28161637
36. endocortical resorption is driven by reduced osteoprotegerin rather than elevated RANKL expression PMID: 27460899
37. The results showed that AG490 inhibited (p)-JAK2 and RANKL expression. PMID: 28278513
38. Play a supportive role in the RANKL-dependent differentiation. PMID: 27413168
39. increased expression of RANKL in heterogeneous bone marrow cells provoked bone destruction during Group A Streptococcus infection. PMID: 26894505
40. beta-lapachone inhibits RANKL-induced osteoclastogenesis and could be considered a potent inhibitor of RANKL-mediated bone diseases PMID: 27913299
41. differentiation by suppressing the Ca(2+)-calcineurin-NFATc1 signaling pathway. Although many questions remain unresolved, to our knowledge, this is the first report demonstrating that PEMF is beneficial against RANKL-dependent osteoclastic differentiation in RAW264.7 cells in vitro via inhibiting the Ca(2+)-calcineurin-NFATc1 signaling pathway. PMID: 27856256
42. these results demonstrate that RANKL expressed by osteocytes is required for the bone loss as well as the increase in B cell number caused by estrogen deficiency. PMID: 27733688
43. In conclusion, the present study demonstrated that EA can suppress osteoclastogenesis in vitro. Moreover, we clarified that these inhibitory effects of EA occur through suppression of NF-kappaB and ERK activation. Therefore, EA may be a potential agent in the treatment of osteoclast-related diseases such as osteoporosis. PMID: 27349866
44. MDH1 expression was induced by receptor activator of nuclear factor kappa-B ligand (RANKL) treatment. PMID: 27179783
45. miR-338-3p may play a significant role in glucocorticoid-induced osteoclast differentiation and function by targeting RANKL in osteoclasts. PMID: 27706599
46. the protein and RNA levels of RANKLinduced cFos and nuclear factor of activated T-cell cytoplasmic 1 were suppressed by centipedegrass extract (CGE). These results indicated that CGE may serve as a useful drug in the prevention of bone loss. PMID: 27035226
47. Lipopolysaccharides significantly up-regulated RANKL expression and activated the ERK1/2 pathway to induce IL-6 mRNA expression and protein synthesis in MLO-Y4 cells. PMID: 27778412
48. this study shows that OPG constitutes an early biomarker with in experimental model od severe malaria PMID: 26766771
49. Osteoprotegerin plays a role in preserving myocardial structure and function with ageing through a reduction in apoptosis and preservation of the matrix structure PMID: 26825553
50. These results indicate that activation of Panx1 and P2X7 R are required for apoptotic osteocytes in fatigued bone to trigger RANKL production in neighboring bystander osteocytes and implicate ATP as an essential signal mediating this process. PMID: 26553756

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KEGG: mmu:21943

STRING: 10090.ENSMUSP00000022592

UniGene: Mm.249221