Anti-RANKL Magnetic Beads-IP Kit Product Components
Components | Storage |
Anti-RANKL Magnetic Beads1,3 | 2-8℃ for 12 months |
NP40 Cell Lysis Buffer2 | -20℃ for 12 months |
5×TBST(pH7.4) | |
1×TBST(pH7.4) | |
ddH2O | |
CD166 Positive Cell Lysate | -20℃ for 12 months |
Alkaline Elution Buffer | 2-8℃ for 12 months |
Acidity Elution Buffer | 2-8℃ for 12 months |
Neutralization Buffer | 2-8℃ for 12 months |
[1] The IP KIT contains anti-RANKL magnetic Beads (2 mg/mL) in phosphate buffered saline (PBS, pH 7.4) with sodium azide (0.1%).
[2] Using NP-40 cell lysate buffer in the kit is required,otherwise,the magnetic beads may be precipitated.
[3] Shipping: Magnetic Beads kits are shipped at ambient temperature in which magnetic beads are provided in liquid buffer.
Anti-RANKL Magnetic Beads-IP Kit Product Description
The Anti-RANKL magnetic Beads, conjugated with Anti-RANKL antibody, are used for immuneprecipitation (IP) of RANKL proteins which expressed in vitro expression systems. For IP, the beads are added to a sample containing RANKL proteins to form a bead-protein complex. The complex is removed from the solution manually using a magnetic separator. The bound RANKL proteins are dissociated from the magnetic beads using an elution buffer. Anti-RANKL Magnetic Beads-IP Kit Antibody Information
Immunogen
Recombinant Human RANKL / OPGL / TNFSF11 / CD254 protein (Catalog#11682-HNCH)
Species Reactivity
Human RANKL / OPGL / TNFSF11 /
Source
Monoclonal Human Rabbit IgG
Preparation
This antibody was obtained from a rabbit immunized with purified, recombinant Human RANKL / OPGL / TNFSF11 / CD254 (rh RANKL / OPGL / TNFSF11 / CD254; Catalog#11682-HNCH; O14788-2; Gly63-Asp244).
Applications
Immunoprecipitation (IP), Minimum Protein Purification
Anti-RANKL Magnetic Beads Immunoprecipitation (IP) Kit Alternative Names
Anti-CD254ALCAM Magnetic Beads-Immunoprecipitatiopn (IP) Kit;Anti-hRANKL2ALCAM Magnetic Beads-Immunoprecipitatiopn (IP) Kit;Anti-ODFALCAM Magnetic Beads-Immunoprecipitatiopn (IP) Kit;Anti-OPGLALCAM Magnetic Beads-Immunoprecipitatiopn (IP) Kit;Anti-OPTB2ALCAM Magnetic Beads-Immunoprecipitatiopn (IP) Kit;Anti-RANKLALCAM Magnetic Beads-Immunoprecipitatiopn (IP) Kit;Anti-sOdfALCAM Magnetic Beads-Immunoprecipitatiopn (IP) Kit;Anti-TRANCEALCAM Magnetic Beads-Immunoprecipitatiopn (IP) Kit
RANKL Background Information
Tumor necrosis factor ligand superfamily member 11, also known as Receptor activator of nuclear factor kappa-B ligand, Osteoprotegerin ligand, TNFSF11, RANKL, TRANCE, OPGL and CD254, is a single-pass type II membrane protein which belongs to the tumor necrosis factor family. The receptor activator of nuclear factor-kappaB ligand (RANKL), its cognate receptor RANK, and its natural decoy receptor osteoprotegerin have been identified as the final effector molecules of osteoclastic bone resorption. RANK and RANKL are key regulators of bone remodeling and regulate T cell/dendritic cell communications, and lymph node formation. Moreover, RANKL and RANK are expressed in mammary gland epithelial cells and control the development of a lactating mammary gland during pregnancy. Genetically, RANKL and RANK are essential for the development and activation of osteoclasts and bone loss in response to virtually all triggers tested. Inhibition of RANKL function via the natural decoy receptor osteoprotegerin (OPG, TNFRSF11B) prevents bone loss in postmenopausal osteoporosis and cancer metastases. Importantly, RANKL appears to be the pathogenetic principle that causes bone and cartilage destruction in arthritis. RANK-RANKL signaling not only activates a variety of downstream signaling pathways required for osteoclast development, but crosstalk with other signaling pathways also fine-tunes bone homeostasis both in normal physiology and disease. In addition, RANKL and RANK have essential roles in lymph node formation, establishment of the thymic microenvironment, and development of a lactating mammary gland during pregnancy.
Immune Checkpoint Immunotherapy Cancer Immunotherapy Targeted Therapy Full Name
tumor necrosis factor (ligand) superfamily, member 11
References
Takayanagi H, et al. (2002) Signaling crosstalk between RANKL and interferons in osteoclast differentiation. Arthritis Res. 4 Suppl 3: S227-32. Nakashima T, et al. (2003) RANKL and RANK as novel therapeutic targets for arthritis. Curr Opin Rheumatol. 15(3): 280-7. Schwarz EM, et al. (2007) Clinical development of anti-RANKL therapy. Arthritis Res Ther. 9 Suppl 1: S7. Leibbrandt A, et al. (2008) RANK/RANKL: regulators of immune responses and bone physiology. Ann N Y Acad Sci. 1143: 123-50.