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Recombinant Rat TNF-α (carrier-free)
Recombinant Rat TNF-α (carrier-free)
580102
10 µg
¥30,000
580104
25 µg
¥59,000
580106
100 µg
¥150,000
580108
500 µg
¥360,000
Product Details
Source:
Rat TNF-α, amino acids Leu80-Leu235 (Accession # NM_012675) was expressed in E. coli.
Formulation:
0.22µm filtered protein solution is in 10mM NaH2PO4, 150mM NaCl, pH 7.2.
Endotoxin Level:
Endotoxin level is <0.1 EU/µg (<0.01 ng/µg) protein as determined by the LAL method.
Preparation:
10-100µg sizes are bottled at 200µg/mL. 500µg sizes and larger are bottled at the concentration indicated on the vial.
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 10µg/mL in buffer containing carrier protein such as 1% BSA or HSA or 10% FBS. For long term-storage, aliquot into polypropylene vials and store in a manual defrost freezer. Avoid repeated freeze/thaw cycles.
Activity:
The ED50 is 5- 15 pg/ml, corresponding to a specific activity of 2 - 0.66 x 108units/mg, as determined by a dose dependent cytotoxicity assay using L929 cells treated with actinomycin D.
TNF-α was originally described as an endotoxin-induced, macrophage-derived factor that promotes hemorrhagic necrosis of solid tumors and the cachexia of chronic infections. TNF-α has also been implicated in a range of inflammatory, infectious, and malignant disorders. At the cellular level, TNF-α modulates a broad spectrum of responses including inflammation, immunoregulation, proliferation, apoptosis, and antiviral activity. In bone, the cytokine inhibits extracellular matrix deposition, stimulates matrix metalloprotease synthesis, and enhances production of osteoclastogenic cytokines such as M-CSF and RANKL. Chronic exposure to TNFa in vivo increases osteoclastogenesis through two distinct mechanisms. TNFa first affects osteoclastogenesis at the osteoclast precursor stage in the bone marrow by priming these cells to differentiate into cFms+/CD11b+/RANK+/- osteoclast progenitors via a RANKL/RANK independent mechanism. These osteoclast precursors then enter the blood and peripheral tissues where they differentiate into mature osteoclasts in the presence of RANKL, and this process is accelerated by TNF. The role of TNF at this later stage of osteoclast differentiation is RANKL/RANK dependent. Importantly, TNF-α promotes bone resorption both in vitro and in vivo by enhancing the proliferation and differentiation of osteoclast precursors.
It is produced primarily by macrophages, and it is also be expressed by activated T cells, B cells, NK cells, and neutrophils.
Function:
Type II integral membrane protein processed by TACE for secretion; upregulated by interferons, IL-2, GM-CSF, substance P, bradykinin, PAF, immune complexes, cyclooxygenase; downregulated by IL-6, TGF-β, vitamin D3, prostaglandin E2, PAF antagonists
Ligand Receptor:
TNFRSF1A (TNF-R1, CD120a, TNFR-p60 Type β, p55); TNFRSF1B (TNF-R2, CD120b, TNFR-p80 Type A, p75)
*These products may be covered by one or more Limited Use Label Licenses (see the BioLegend Catalog or our website, www.biolegend.com/terms). BioLegend products may not be transferred to third parties, resold, modified for resale, or used to manufacture commercial products or to provide a service to third parties without written approval of BioLegend. By use of these products you accept the terms and conditions of all applicable Limited Use Label Licenses. Unless otherwise indicated, these products are for research use only and are not intended for human or animal diagnostic, therapeutic or commercial use.
