RANKL and RANK are members of the TNF superfamily of ligands and receptors that play an important role in the regulation of specific immunity and bone turnover. RANK (receptor) was originally identified as a dendritic cell-membrane protein, which, by interacting with RANKL, augments the ability of dendritic cells. These dendritic cells then stimulate naïve T-cell proliferation in a mixed lymphocyte reaction, promote the survival of RANK+ T-cells, and regulate T-cell-dependent immune response. RANKL, which is expressed in a variety of cells, including osteoblasts, fibroblasts, activated T-cells and bone marrow stromal cells, is also capable of interacting with a decoy receptor called OPG. Binding of soluble OPG to sRANKL inhibits osteoclastogenesis by interrupting the signaling between stromal cells and osteoclastic progenitor cells, thereby leading to excess accumulation of bone and cartilage. Human RANKL is reactive on murine cells. Recombinant Human sRANKL is a 20.0 kDa polypeptide comprising the TNF-homologous region of RANKL (176 amino acid residues).
soluble Receptor Activator of NF-κB Ligand, TNFSF11, TRANCE (TNF-related activation-induced cytokine), OPGL, ODF (Osteoclast differentiation factor)
MEKAMVDGSW LDLAKRSKLE AQPFAHLTIN ATDIPSGSHK VSLSSWYHDR GWAKISNMTF SNGKLIVNQD GFYYLYANIC FRHHETSGDL ATEYLQLMVY VTKTSIKIPS SHTLMKGGST KYWSGNSEFH FYSINVGGFF KLRSGEEISI EVSNPSLLDP DQDATYFGAF KVRDID
≥ 98% by SDS-PAGE gel and HPLC analyses.
Determined by its dose-dependent ability to induce reporter gene in HT-29 NF-κB Luc reporter cells.
Calculated Molecular Weight:
Endotoxin level is < 0.1 ng/ug of protein (< 1 EU/ug)
Not for human use.