sRANK Ligand Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application ![]()
| WB, IHC-P, E |
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Primary Accession | O14788 |
Other Accession | NP_003692, 4507595 |
Reactivity | Human, Mouse, Rat |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | IgG |
Calculated MW | 35 kDa |
Application Notes | sRANK-L antibody can be used for detection of sRANK-L by Western blot at 0.25 - 0.5 µg/mL. Antibody can also be used for immunohistochemistry starting at 5 µg/mL. |
Gene ID | 8600 |
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Other Names | sRANK Ligand Antibody: ODF, OPGL, sOdf, CD254, OPTB2, RANKL, TRANCE, hRANKL2, Tumor necrosis factor ligand superfamily member 11, Osteoclast differentiation factor, ODF, tumor necrosis factor (ligand) superfamily, member 11 |
Target/Specificity | TNFSF11; |
Reconstitution & Storage | Antibody can be stored at 4°C up to one year. Antibodies should not be exposed to prolonged high temperatures. |
Precautions | sRANK Ligand Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | TNFSF11 |
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Synonyms | OPGL, RANKL, TRANCE |
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 (PubMed:22664871). 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 (By similarity). |
Cellular Location | [Isoform 1]: Cell membrane; Single-pass type II membrane protein [Isoform 2]: Cytoplasm. |
Tissue Location | Highest in the peripheral lymph nodes, weak in spleen, peripheral blood Leukocytes, bone marrow, heart, placenta, skeletal muscle, stomach and thyroid |

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Provided below are standard protocols that you may find useful for product applications.
Background
sRANK Ligand Antibody: The receptor activator of NF-κB ligand (RANK-L) is a recently discovered member of the TNF-ligand family involved in the regulation of the T cell-dependent immune response, lymph node organogenesis and bone formation. RANK-L exists as both a normal, transmembrane form and a truncated, soluble form (sRANK-L), both of which can stimulate the receptor. Activation of T cells, such as by treatment with interleukin-7, induces RANK-L production and leads to an increase of osteoclast formation and bone loss. Finally, sRANK-L can activate the antiapoptotic kinase Akt through a signaling complex involving Src kinase and TRAF6, suggesting sRANK-L may also play a role in regulating apoptosis. This antibody will recognize both the soluble form and the uncleaved transmembrane form of RANK-L.
References
Wong BR, Rho J, Arron J, et al. TRANCE is a novel ligand of the tumor necrosis factor receptor family that activates c-Jun N-terminal kinase in T cells. J. Biol. Chem. 1997; 272:25190-4.
Kong YY, Yoshida H, Sarosi I, et al. OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node organogenesis. Nature 1999; 397:315-23.
Weitzmann MN, Cenci S, Rifas L, et al. Interleukin-7 stimulates osteoclast formation by up-regulating the T-cell production of soluble osteoclastogenic cytokines. Blood 2000; 96:1873-8.
Bharti AC, Takada Y, Shishodia S, et al. Evidence that receptor activator of the nuclear factor (NF)-kappaB ligand can suppress cell proliferation and induce apoptosis through activation of a NF-kappaB-independent and TRAF6-dependent mechanism. J. Biol. Chem. 2004; 279:6065-76.

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