TNF alpha Protein (AA 80-235)
Quick Overview for TNF alpha Protein (AA 80-235) (ABIN2666709)
Target
See all TNF alpha ProteinsProtein Type
Biological Activity
Origin
Source
Application
Purity
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Protein Characteristics
- AA 80-235
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Sterility
- 0.22 μm filtered
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Endotoxin Level
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Endotoxin level is <0.1 EU/μg (<0.01 ng/μg) protein as determined by the LAL method.
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Application Notes
- Optimal working dilution should be determined by the investigator.
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Comment
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Biological 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.
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Restrictions
- For Research Use only
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Format
- Liquid
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Reconstitution
- For maximum results, quick spin vial prior to opening. The protein can be aliquoted and stored from -20 °C to -70 °C. Stock solutions can also be prepared at 50-100 μg/mL in sterile buffer (PBS, HPBS, DPBS, or EBSS) containing carrier protein such as 0.2-1 % BSA or HSA and stored in working aliquots at -20 °C to -70 °C.
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Buffer
- 0.22μm filtered protein solution is in 10 mM NaH2PO4, 150 mM NaCl, pH 7.2.
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Handling Advice
- Avoid repeated freeze/thaw cycles.
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Storage
- -20 °C
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Storage Comment
- Unopened vial can be stored between 2°C and 8°C for one month, at -20°C for six months, or at -70°C for one year.
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- TNF alpha (Tumor Necrosis Factor alpha (TNF alpha))
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Alternative Name
- TNF-alpha
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Background
- 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.
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Molecular Weight
- The 157 amino acid N-terminal methionylated recombinant protein has a predicted molecular mass of approximately 17,361 Da. The DTT-reduced protein migrates at approximately 17kDa and the non-reduced protein migrates at approximately 16kDa by SDS-PAGE.
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Pathways
- NF-kappaB Signaling, Apoptosis, Caspase Cascade in Apoptosis, TLR Signaling, Cellular Response to Molecule of Bacterial Origin, Regulation of Leukocyte Mediated Immunity, Positive Regulation of Immune Effector Process, Production of Molecular Mediator of Immune Response, Positive Regulation of Endopeptidase Activity, Hepatitis C, Protein targeting to Nucleus, Inflammasome
Target
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