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Recombinant Mouse TRANCE (RANKL) (carrier-free)
Recombinant Mouse TRANCE (RANKL) (carrier-free)
577102
10 µg
¥40,000
Product Details
Source:
Mouse TRANCE, amino acids Lis158-Asp316 (Accession # NM_011613.3) was expressed in insect cells, with an N-terminal 9-His tag and IEGR-Xa sequence.
Formulation:
0.22 µm filtered protein solution is in PBS
Endotoxin Level:
Less than 0.01 ng per µg cytokine as determined by the LAL method.
Preparation:
Bottled at 0.2 mg/ml.
Storage & Handling:
Unopened vial can be stored at 4°C for three months, at -20°C for six months, or at -70°C for one year. For maximum results, quick spin vial prior to opening. Stock solutions should be prepared at no less than 10 µg/mL in sterile buffer containing carrier protein such as 1% BSA or HSA or 10% FBS. After dilution, the cytokine can be stored at 4°C for one month or from -20°C to -70°C for up to 3 months. Avoid repeated freeze/thaw cycles.
Activity:
Bioactivity was measured by its property to induce osteoclast differentiation in RAW264.7 cells in the absence of any cross-linking. The bioactivity is equivalent to competitor cytokines.
RANKLgene encodes a type II membrane protein of 316 amino acids with a predicted molecular mass of 35 kD.RANKL is cleaved to produce a soluble form with biological activity. The shedding of membrane-bound RANKL appears to be mediated by expression of matrix metalloproteinase (MMP) 14 and ADAM10. Suppression of MMP14 in primary osteoblasts increases membrane-bound RANKL and promotes osteoclastogenesis in cocultures with macrophages. Therefore, RANKL shedding seems to be an important process that down-regulates local osteoclastogenesis. Alternatively, an increased production of RANKL by osteoblastic cells leads to osteoclast differentiation, activation, and survival, which results in increased bone resorption. Binding of RANKL to its receptor RANK activates TNF receptor- associated factor 6 (TRAF6), which is linked to downstream pathways including NF-kB, c-jun N-terminal kinase (JNK) or Src. TRAF6 has been shown to be necessary for the differentiation of osteoclastic cells by enhancing Src kinase, essential for osteoclast function.
T cells, osteoblasts, bone marrow stromal cells, hypertrophic and prehypertrophic chondrocytes, stromal fibroblasts, synovial cells, and megakaryocytes.
Function:
RANKL is a potent stimulator of osteoclast formation from precursor cells and bone-resorbing activity in mature osteoclasts. The expression of RANKL in human and murine osteoblastic cells is stimulated by various cytokines (IL-1, TNFa and IL-11) and calciotrophic hormones including PTH, 1,25dihydroxyvitamin D3 (1,25D3) and prostaglandin E2. RANKL augments the ability of dendritic cells to stimulate naïve T-cell proliferation. RANKL activates JNK and NF-κB and induces the expression of IL-1, IL-6, IL-12, and IL-15 in dendritic cells. In addition, RANKL is a crucial factor in lymphocyte development and lymph node organogenesis. RANKL stimulates proliferation, adhesion, and IL-7 expression of thymic epithelial cells.
Ligand Receptor:
TNFRSF11A (Tumor necrosis factor receptor superfamily, member 11A) also called RANK and TNFRSF11B (OPG) which acts as a decoy receptor for RANKL and as a potent inhibitor of osteoclast formation.
Interaction:
T cells, dendritic cells, bone marrow derived macrophages, osteoclast precursors and mature osteoclasts.
Antigen References:
1. Dehm SM, et al. 2004. Biochem. Cell Biol. 82:263. 2. Hikita A, et al. 2006. J. Biol. Chem. 281:36846. 3. Kim NS, et al. 2006. Mol. Cell. Biol. 26:1002. 4. Wada T, et al. 2006. TRENDS Mol. Med. 12:17. 5. Lee HW, et al. 2008. Exp. Mol. Med. 40:59. 6. Ha J, et al. 2010. J. Immunol. 184:4717.
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