SRP3161
sRANKL human
recombinant, expressed in E. coli, ≥98% (SDS-PAGE), ≥98% (HPLC), suitable for cell culture
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ODF (Osteoclast differentiation factor), TNFSF11, TRANCE (TNF-related activation-induced cytokine), soluble Receptor Activator of NFkB Ligand
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biological source
human
recombinant
expressed in E. coli
Assay
≥98% (HPLC)
≥98% (SDS-PAGE)
form
lyophilized
potency
10.0-25.0 ng/mL ED50
mol wt
20.0 kDa
packaging
pkg of 10 μg
technique(s)
cell culture | mammalian: suitable
impurities
<0.1 EU/μg endotoxin, tested
color
white
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
Gene Information
human ... TNFSF11(8600)
General description
TRANCE (TNF-related activation-induced cytokine), also known as sRANKL (soluble receptor activator of nuclear factor K-B ligand), is encoded by the gene mapped to human chromosome 13q14.11. sRANKL and RANK (receptor activator of nuclear factors-KB) are members of the tumor necrosis factor (TNF) superfamily of ligands and receptors that play an important role in the regulation of specific immunity and bone turnover. RANKL is expressed in a variety of cells including osteoblasts, fibroblasts, activated T-cells and bone marrow stromal cells. Recombinant human sRANKL is a 20kDa polypeptide comprising the TNF homologous region of RANKL (176 amino acid residues).
Application
sRANKL has been used to initiate differentiation of osteoclasts.
Biochem/physiol Actions
RANKL (receptor activator of nuclear factor K-B ligand) is a potent stimulator of bone resorption. Aberrations in RANK (Receptor activator of nuclear factors-κB) and RANKL (Receptor activator of nuclear factors-κB ligand) genes have been associated with osteoporosis, chronic inflammatory arthritis, the osteolytic bony metastasis of malignancies, and reduced bone mineral density in patients with ankylosing spondylitis. RANK (receptor) was originally identified as a dendritic-cell-membrane protein, which by interacting with RANKL augments the ability of dendritic cells to stimulate naïve T-cell proliferation in a mixed lymphocyte reaction, to promote the survival of RANK+ T cells, and to regulate T-cell-dependent immune response. RANKL is also capable of interacting with a decoy receptor called OPG (osteoprotegerin). 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.
Sequence
MEKAMVDGSW LDLAKRSKLE AQPFAHLTIN ATDIPSGSHK VSLSSWYHDR GWAKISNMTF SNGKLIVNQD GFYYLYANIC FRHHETSGDL ATEYLQLMVY VTKTSIKIPS SHTLMKGGST KYWSGNSEFH FYSINVGGFF KLRSGEEISI EVSNPSLLDP DQDATYFGAF KVRDID
Physical form
Lyophilized from 5 mM Sodium Phosphate, pH 7.6 + 75 mM NaCl.
Reconstitution
Centrifuge the vial prior to opening. Reconstitute in water to a concentration of 0.1-1.0 mg/ml. Do not vortex. This solution can be stored at 2-8°C for up to 1 week. For extended storage, it is recommended to further dilute in a buffer containing a carrier protein (example 0.1% BSA) and store in working aliquots at -20°C to -80°C.
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Regulatory Information
常规特殊物品
Certificates of Analysis (COA)
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Cost-effective analysis of candidate genes using htSNPs: a staged approach.
Genes and Immunity, 5(4), 301-301 (2004)
The role of osteoprotegerin and receptor activator of nuclear factor KB ligand in the pathogenesis and treatment of rheumatoid arthritis.
Arthritis & Rheumatology (Hoboken, N.J.), 44(2), 253-259 (2001)
Interactions of tumor necrosis factor (TNF) and TNF receptor family members in the mouse and human.
The Journal of Biological Chemistry, 281(20), 13964-13971 (2006)
EGF-like ligands stimulate osteoclastogenesis by regulating expression of osteoclast regulatory factors by osteoblasts: implications for osteolytic bone metastases.
The Journal of Biological Chemistry, 282, 26656-26664 (2007)
Elevated serum levels of soluble receptor activator of nuclear factors-kappaB ligand (sRANKL) and reduced bone mineral density in patients with ankylosing spondylitis (AS).
Rheumatology (Oxford, England), 45, 1197-1200 (2006)
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