Product Pathways - NF-kB Signaling
RANK Ligand (R2) Antibody #3959
|3959S||100 µl (10 western blots)||---||In Stock||---|
|3959||carrier free and custom formulation / quantity||email request|
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Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IP=Immunoprecipitation
Species predicted to react based on 100% sequence homology: Monkey, Bovine, Pig.
Specificity / Sensitivity
RANK Ligand (R2) Antibody detects transfected levels of cellular RANK Ligand protein.
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human RANK Ligand, within the cytoplasmic region. Antibody was purified by protein A and peptide affinity chromatography.
RANK (receptor activator of NF-κB) is a member of the tumor necrosis factor (TNF) receptor subfamily that is activated by its ligand, RANKL (TRANCE/OPGL/ODF), to promote survival of dendritic cells and differentiation of osteoclasts (1-4). Although RANK is widely expressed, its cell surface expression may be more restricted to dendritic cells and foreskin fibroblasts (1). RANK contains a 383-amino acid intracellular domain that associates with specific members of the TRAF family to NF-κB and JNK activiation (1,5). RANKL/RANK signaling may also lead to survival signaling through activation of the Akt pathway and an upregulation of survival proteins, including Bcl-xL (2,6). RANK signaling has been implicated as a potential therapeutic to inhibit bone loss and arthritis (7,8).
RANKL (1), also named TNF-related activation-induced cytokine (TRANCE) (2,9), osteoprotegerin ligand (OPGL) (3), osteoclast differentiation factor (ODF) (4), and TNFSF11, is a type II transmembrane protein of the TNF family that exists as both a membrane-bound and soluble form. It is an essential regulator of immune function and bone development and homeostasis (7,10,11). RANKL is predominately expressed in activated T cells, as well as the thymus, lymph node, and bone marrow and promotes dendritic cell survival. Deletion of RANKL in mice leads to severe osteoporosis with a loss of osteoclasts, defects in T and B cell differentiation, loss of lymph node development, and mammary gland development during pregnancy (12-14).
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