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AB83145

Biotin Anti-sRANKL antibody

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(1 Publication)

Rabbit Polyclonal RANKL antibody - conjugated to Biotin. Suitable for WB, sELISA and reacts with Recombinant full length protein - Human samples. Cited in 1 publication. Immunogen corresponding to Recombinant Full Length Protein corresponding to Human TNFSF11.

View Alternative Names

CD254, OPGL, RANKL, TRANCE, TNFSF11, Tumor necrosis factor ligand superfamily member 11, Osteoclast differentiation factor, Osteoprotegerin ligand, Receptor activator of nuclear factor kappa-B ligand, TNF-related activation-induced cytokine, ODF

2 Images
Sandwich ELISA - Biotin Anti-sRANKL antibody (AB83145)
  • sELISA

Supplier Data

Sandwich ELISA - Biotin Anti-sRANKL antibody (AB83145)

To detect human sRANKL by sandwich ELISA (using 100 μl/well antibody solution) a concentration of 0.25 – 1.0 μg/ml of ab83145 is required. This biotinylated polyclonal antibody, in conjunction with an anti-RANKL (ab9957) as a capture antibody, allows the detection of at least 0.2 – 0.4 ng/well of recombinant human sRANKL.

Western blot - Biotin Anti-sRANKL antibody (AB83145)
  • WB

Supplier Data

Western blot - Biotin Anti-sRANKL antibody (AB83145)

To detect human sRANKL by Western Blot analysis ab83145 can be used at a concentration of 0.1 - 0.2 μg/ml. Used in conjunction with compatible secondary reagents the detection limit for recombinant human sRANKL is 1.5 - 3.0 ng/lane, under either reducing or non-reducing conditions.

Image shown is non-reducing conditions; Human recombinant sRANKL protein at 250 - 0.24 ng/ml.

Lane 1 is MW marker, lanes 2-12 human recombinant sRANKL protein.

All lanes:

Western blot - Biotin Anti-sRANKL antibody (ab83145)

Predicted band size: 35 kDa

false

Key facts

Host species

Rabbit

Clonality

Polyclonal

Isotype

IgG

Conjugation

Biotin

Excitation/Emission
Carrier free

No

Applications

WB, sELISA

applications

Immunogen

Recombinant Full Length Protein corresponding to Human TNFSF11.

O14788

Reactivity data

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Properties and storage information

Form
Lyophilized
Reconstitution
Centrifuge vial prior to opening. Reconstitute in 50 µl sterile PBS containing 0.1% BSA to give a concentration of 1.0 mg/ml.
Purification technique
Affinity purification Immunogen
Purification notes
ab83145 is sterile filtered. ab83145 was purified by affinity chromatography and then biotinylated.
Storage buffer
Constituents: PBS
Shipped at conditions
Blue Ice
Appropriate short-term storage duration
1-2 weeks
Appropriate short-term storage conditions
+4°C
Appropriate long-term storage conditions
-20°C
Storage information
Avoid freeze / thaw cycle

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

SRANKL also known as soluble receptor activator of nuclear factor kappa-B ligand is an essential protein involved in bone metabolism. It acts as a cytokine and is a member of the tumor necrosis factor (TNF) superfamily. sRANKL is derived from the membrane-bound form of RANKL by proteolytic cleavage and has a molecular weight of approximately 18 kDa. This protein is predominantly found in osteoblasts osteocytes and T-cells where it plays a critical role in physiological processes.
Biological function summary

SRANKL facilitates the differentiation and activation of osteoclasts which are cells responsible for bone resorption. It binds to its receptor RANK on osteoclast precursors promoting their maturation into fully functional osteoclasts. This binding process involves complex formation and interaction with another molecule called osteoprotegerin (OPG) which acts as a decoy receptor regulating sRANKL activity and therefore controlling bone resorption.

Pathways

SRANKL plays a fundamental role in the RANK/RANKL/OPG signaling pathway which is important for maintaining bone homeostasis. This pathway regulates the balance between bone formation and resorption. It also interacts with NF-kappaB signaling a pathway that influences inflammation and immune response. sRANKL through these pathways closely connects with proteins such as TRAF6 which mediates downstream signaling leading to osteoclastogenesis.

Alterations in the sRANKL pathway impact bone-related diseases such as osteoporosis and rheumatoid arthritis. In osteoporosis increased levels of sRANKL enhance osteoclast activity leading to excessive bone resorption and thereby weakening bones. In rheumatoid arthritis the interaction between sRANKL and RANK promotes inflammation and joint destruction. This protein is linked to OPG as variations in their ratio influence disease development and progression.

Product protocols

For this product, it's our understanding that no specific protocols are required. You can visit:

Target data

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).
See full target information TNFSF11

Publications (1)

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Experimental dermatology 32:403-412 PubMed36457234

2022

CCL6 promotes M2 polarization and inhibits macrophage autophagy by activating PI3-kinase/Akt signalling pathway during skin wound healing.

Applications

Unspecified application

Species

Unspecified reactive species

Xiao Feng,Yu Ji,Ce Zhang,Tingting Jin,Jingyu Li,Jincai Guo
View all publications

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