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Key Documents

T8300

Sigma-Aldrich

Anti-Tumor Necrosis Factor-α antibody produced in rabbit

IgG fraction of antiserum, buffered aqueous solution

Synonym(s):

Anti-TNF-α

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About This Item

MDL number:
UNSPSC Code:
51111800
NACRES:
NA.41

biological source

rabbit

conjugate

unconjugated

antibody form

IgG fraction of antiserum

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

species reactivity

human

technique(s)

dot blot: 1:2,000
microarray: suitable
neutralization: 1-3 μg/mL

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... TNF(7124)

General description

Tumor necrosis factor- α(TNF-α), also known as cachectin, is an inflammatory cytokine that exists primarily as a 51kDa complex built up of 3 identical, non-covalently-linked polypeptide subunits (17 kDa, 157 amino acid residues, in human). TNF- αoccurs as a secreted, soluble form and as a membrane-anchored form, both of which are biologically active. TNF-α is secreted by neutrophils, activated lymphocytes, macrophages, NK cells, LAK cells, astrocytes, endothelial cells, smooth muscle cells, and some transformed cells.

Specificity

The antibody binds to TNF-α. It does not cross-react with recombinant human TNF-β, IL-1a, IL-1β or IL-3, nor with recombinant mouse or human IL-6.

Immunogen

recombinant human TNF-α produced in bacteria.

Application

Anti-Tumor Necrosis Factor-α antibody may be used for dot blot at a working antibody dilution of 1:2000. The antibody may be used for neutralization assay; the ND50 is 1-3 μg/ml. Anti-TNF-α antibody was used for neutralization of TNF-α of Jurkat cells.
Anti-Tumor Necrosis Factor-α antibody produced in rabbit has been used in western blotting. It may also be used in enzyme linked immunoassay (ELISA).

Biochem/physiol Actions

Tumor Necrosis Factor-α (TNF-α) is a cytokine produced by macrophages in response to stimulus by LPS. It plays a major role in mediating inflammation, tissue injury, pathogenic shock, innate immunity, apoptosis and autoimmunity. The physiological effects of TNF-α are mediated by receptors of TNFR super family. The TNF/TNFR signaling axis plays a critical role in mediating either survival or apoptosis depending on the class of adaptor proteins recruited in the cell. Association of receptors with a death domain causes rapid activation of caspases and results in cell death. TNF/TNFR also results in the activation of downstream pathways involving MAPK, p38, JNK and NF-κB that play a major role in innate immunity, acute inflammatory responses and homeostasis. The TNF/TNFR axis is also important in the pathology of various autoimmune and inflammatory disorders including a variety of malignancies and Alzheimer′s disease.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class

12 - Non Combustible Liquids

wgk_germany

nwg

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Transmembrane TNF-alpha: structure, function and interaction with anti-TNF agents
Horiuchi T, et al.
Rheumatology (Basel), 49(7), 1215-1228 (2010)
Z Han et al.
The Journal of biological chemistry, 276(42), 38748-38754 (2001-08-22)
Non-steroidal anti-inflammatory drugs (NSAIDs) are inhibitors of cyclooxygenase-1 and -2 and are useful for prevention and cure of cancers, especially colon and rectal cancers. The NSAIDs indomethacin and sulindac sulfide have been shown to induce apoptosis of colon epithelial cancer
Tumor necrosis factor
Chu WM, et al.
Cancer Letters, 328(2), 222-225 (2013)
K A Papadakis et al.
Annual review of medicine, 51, 289-298 (2000-04-25)
Recent advances in the drug treatment of inflammatory bowel disease (IBD) have paralleled our understanding of the pathophysiology of ulcerative colitis and Crohn's disease. Several proinflammatory and immune-regulatory cytokines are upregulated in the mucosa of patients with IBD, and differences
The TNF receptor superfamily of cellular and viral proteins: activation, costimulation, and death.
C A Smith et al.
Cell, 76(6), 959-962 (1994-03-25)

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