Product Details

Purity

Greater than 90% as determined by SDS-PAGE.

Target Names

Tnfsf11

Uniprot No.

O35235

Research Area

Others

Alternative Names

Tnfsf11; Opgl; Rankl; Trance; Tumor necrosis factor ligand superfamily member 11; Osteoclast differentiation factor; ODF; Osteoprotegerin ligand; OPGL; Receptor activator of nuclear factor kappa-B ligand; RANKL; TNF-related activation-induced cytokine; TRANCE; CD antigen CD254) [Cleaved into: Tumor necrosis factor ligand superfamily member 11; membrane form; Tumor necrosis factor ligand superfamily member 11; soluble form]

Species

Mus musculus (Mouse)

Source

E.coli

Expression Region

70-316aa

Target Protein Sequence

YFRAQMDPNRISEDSTHCFYRILRLHENADLQDSTLESEDTLPDSCRRMKQAFQGAVQKELQHIVGPQRFSGAPAMMEGSWLDVAQRGKPEAQPFAHLTINAASIPSGSHKVTLSSWYHDRGWAKISNMTLSNGKLRVNQDGFYYLYANICFRHHETSGSVPTDYLQLMVYVVKTSIKIPSSHNLMKGGSTKNWSGNSEFHFYSINVGGFFKLRAGEEISIQVSNPSLLDPDQDATYFGAFKVQDID
Note: The complete sequence may include tag sequence, target protein sequence, linker sequence and extra sequence that is translated with the protein sequence for the purpose(s) of secretion, stability, solubility, etc.
If the exact amino acid sequence of this recombinant protein is critical to your application, please explicitly request the full and complete sequence of this protein before ordering.

Mol. Weight

43.9kDa

Protein Length

Extracellular Domain

Tag Info

N-terminal 6xHis-SUMO-tagged

Form

Liquid or Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.

Buffer

If the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol.
Note: If you have any special requirement for the glycerol content, please remark when you place the order.
If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose.

Reconstitution

We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. Our default final concentration of glycerol is 50%. Customers could use it as reference.

Troubleshooting and FAQs

Protein FAQs

Storage Condition

Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.

Shelf Life

The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.

Lead Time

3-7 business days

Notes

Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.

Datasheet & COA

Please contact us to get it.

Description

Amino acids 70-316 form the expressed segment for recombinant Mouse Tnfsf11. The calculated molecular weight for this Tnfsf11 protein is 43.9 kDa. This Tnfsf11 protein is produced using e.coli expression system. The Tnfsf11 coding gene included the N-terminal 6xHis-SUMO tag, which simplifies the detection and purification processes of the recombinant Tnfsf11 protein in following stages of expression and purification.

Tumor necrosis factor ligand superfamily member 11 (Tnfsf11), also known as RANKL, is a key cytokine involved in the regulation of bone metabolism. It plays a crucial role in the differentiation and activation of osteoclasts, the cells responsible for bone resorption. RANKL binds to its receptor RANK on the surface of osteoclast precursors, triggering a signaling cascade that promotes osteoclast formation, function, and survival. Additionally, RANKL is essential for various physiological processes, including the development of lymph nodes and the mammary gland. Research on Tnfsf11 spans multiple areas, such as bone biology, immune system regulation, and reproductive physiology. In bone biology, investigations focus on understanding how RANKL signaling influences bone remodeling and its implications for diseases like osteoporosis and arthritis. In the immune system, RANKL is involved in the regulation of lymphoid tissue development and the immune response. Moreover, studies exploring the role of RANKL in reproductive physiology highlight its importance in mammary gland development and lactation. Targeting the RANKL/RANK pathway has therapeutic potential for bone-related disorders.

Target Background

Function

Cytokine that binds to TNFRSF11B/OPG and to TNFRSF11A/RANK. Osteoclast differentiation and activation factor. Augments the ability of dendritic cells to stimulate naive T-cell proliferation. May be an important regulator of interactions between T-cells and dendritic cells and may play a role in the regulation of the T-cell-dependent immune response. May also play an important role in enhanced bone-resorption in humoral hypercalcemia of malignancy. Induces osteoclastogenesis by activating multiple signaling pathways in osteoclast precursor cells, chief among which is induction of long lasting oscillations in the intracellular concentration of Ca (2+) resulting in the activation of NFATC1, which translocates to the nucleus and induces osteoclast-specific gene transcription to allow differentiation of osteoclasts. During osteoclast differentiation, in a TMEM64 and ATP2A2-dependent manner induces activation of CREB1 and mitochondrial ROS generation necessary for proper osteoclast generation.

Gene References into Functions

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
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
Deletion of the RANKL D5 enhancer delays the progression of atherosclerotic plaque development and plaque calcification in hypercholesterolemic mice. PMID: 28419519
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
compressive force induced the differentiation of RAW264.7 from increase in RANK and decrease in LGR4 expression. PMID: 29572179
miR-145 expression was inhibited in RANKL-induced osteoclastogenesis PMID: 29577879
LPS increased mRNA and protein expressions of IL-6 and RANKL on day 14 PMID: 28637991
hBD-1 potentiates the induction of in vitro osteoclastogenesis by RANKL via enhanced phosphorylation of the p44/42 MAPKs PMID: 28709835
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
Rankl(-/-) bone marrow-mesenchymal stromal cell displayed reduced clonogenicity and osteogenic capacity. PMID: 28100034
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
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
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
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
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
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
dihydroartemisinin inhibited RANKL-induced NF-kappaB and NFAT activity. PMID: 26684711
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
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
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
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
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
Osteoprotegerin facilitates pulmonary arterial hypertension pathogenesis by regulating pulmonary arterial smooth muscle cell proliferation via integrin alphavbeta3/FAK/AKT signaling pathway. PMID: 28077433
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
Absence of Musashi2 in osteoclast precursors promotes apoptosis and inhibits RANKL-induced NF-kappaB activation, which is essential for osteoclast survival. PMID: 27441652
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
Estrogens and androgens inhibit osteoblast-driven osteoclastogenesis through non-genomic mechanism(s) that entail, MMP-mediated RANKL dissociation from the cell membrane. PMID: 28213978
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
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
RANKL represses the transcription of the E3 ubiquitin ligase RNF146 through an NF-kappaB-related inhibitory element in the RNF146 promoter. PMID: 28287403
This study showed that RANKL favors osteoclastogenesis via attenuation of Nrf2-mediated antioxidant enzyme expression by competing with Bach1 nuclear accumulation. PMID: 27836987
Membrane-bound RANKL induces M cell differentiation and CCL20 expression in the follicle associated epithelium of gut-associated lymphoid tissues. PMID: 28436956
The data show that S. aureus enhances bone resorption and periosteal osteoclast formation by increasing osteoblast RANKL production through TLR2. PMID: 27311019
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
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
endocortical resorption is driven by reduced osteoprotegerin rather than elevated RANKL expression PMID: 27460899
The results showed that AG490 inhibited (p)-JAK2 and RANKL expression. PMID: 28278513
Play a supportive role in the RANKL-dependent differentiation. PMID: 27413168
increased expression of RANKL in heterogeneous bone marrow cells provoked bone destruction during Group A Streptococcus infection. PMID: 26894505
beta-lapachone inhibits RANKL-induced osteoclastogenesis and could be considered a potent inhibitor of RANKL-mediated bone diseases PMID: 27913299
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
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
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
MDH1 expression was induced by receptor activator of nuclear factor kappa-B ligand (RANKL) treatment. PMID: 27179783
miR-338-3p may play a significant role in glucocorticoid-induced osteoclast differentiation and function by targeting RANKL in osteoclasts. PMID: 27706599
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
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
this study shows that OPG constitutes an early biomarker with in experimental model od severe malaria PMID: 26766771
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
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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Involvement in disease

Deficiency in Tnfsf11 results in failure to form lobulo-alveolar mammary structures during pregnancy, resulting in death of newborns. Trance-deficient mice show severe osteopetrosis, with no osteoclasts, marrow spaces, or tooth eruption, and exhibit profound growth retardation at several skeletal sites, including the limbs, skull, and vertebrae and have marked chondrodysplasia, with thick, irregular growth plates and a relative increase in hypertrophic chondrocytes.

Subcellular Location

[Isoform 1]: Cell membrane; Single-pass type II membrane protein.; [Isoform 2]: Cell membrane; Single-pass type II membrane protein.; [Isoform 3]: Cytoplasm.; [Tumor necrosis factor ligand superfamily member 11, soluble form]: Secreted.

Protein Families

Tumor necrosis factor family

Tissue Specificity

Highly expressed in thymus and lymph nodes, but not in non-lymphoid tissues and is abundantly expressed in T-cells but not in B-cells. A high level expression is also seen in the trabecular bone and lung.

Database Links

KEGG: mmu:21943

STRING: 10090.ENSMUSP00000022592

UniGene: Mm.249221

Code	CSB-EP023986MO
MSDS	MSDS Datasheet
Size	US$388
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Image	(Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel.
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Recombinant Mouse Tumor necrosis factor ligand superfamily member 11 (Tnfsf11), partial

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