RANKL rabbit pAb
ENT-A4289
Description
| REF | ENT-A4289 |
|---|---|
| Category | Antibody Polyclonal |
| Description | RANKL rabbit pAb |
| Source | Rabbit |
| Applications | WB;IHC;IF;ELISA |
| Reactivity | Human;Mouse;Rat |
| Reactivity | Human;Mouse;Rat |
| Dilution | Western Blot: 1/500 – 1/2000. IHC-p: 1:100-300 ELISA: 1/20000. IF 1:100-300 Not yet tested in other applications. |
| Immunogen | The antiserum was produced against synthesized peptide derived from the C-terminal region of human TNFSF11. AA range:268-317 |
| Storage Stability | -20°C/1 year |
| Clonality | Polyclonal |
| Isotype | IgG |
| Concentration | 1 mg/ml |
| Observed Band KD | 35kD |
| Human Gene ID | 8600 |
| Human Swiss Prot Nº | O14788 |
| Subcellular Location | [Isoform 1]: Cell membrane; Single-pass type II membrane protein.; [Isoform 3]: Cell membrane; Single-pass type II membrane protein.; [Isoform 2]: Cytoplasm .; [Tumor necrosis factor ligand superfamily member 11, soluble form]: Secreted . |
Other Name: TNFSF11; OPGL; RANKL; TRANCE; Tumor necrosis factor ligand superfamily member 11; Osteoclast differentiation factor; ODF; Osteoprotegerin ligand; OPGLReceptor activator of nuclear factor kappa-B ligand; RANKL; TNF-related activation-induced cytokine; TRANCE; CD254
Background: This gene encodes a member of the tumor necrosis factor (TNF) cytokine family which is a ligand for osteoprotegerin and functions as a key factor for osteoclast differentiation and activation. This protein was shown to be a dentritic cell survival factor and is involved in the regulation of T cell-dependent immune response. T cell activation was reported to induce expression of this gene and lead to an increase of osteoclastogenesis and bone loss. This protein was shown to activate antiapoptotic kinase AKT/PKB through a signaling complex involving SRC kinase and tumor necrosis factor receptor-associated factor (TRAF) 6, which indicated this protein may have a role in the regulation of cell apoptosis. Targeted disruption of the related gene in mice led to severe osteopetrosis and a lack of osteoclasts. The deficient mice exhibited defects in early differentiation of T and B ly