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T6674

Sigma-Aldrich

Tumor Necrosis Factor-α human

≥97% (SDS-PAGE), recombinant, expressed in E. coli, powder, suitable for cell culture

Synonym(s):

hTNF-α, TNF-α

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About This Item

CAS Number:
MDL number:
UNSPSC Code:
12352202
NACRES:
NA.77

product name

Tumor Necrosis Factor-α human, TNF-α, recombinant, expressed in E. coli, powder, suitable for cell culture

biological source

human

Quality Level

recombinant

expressed in E. coli

Assay

≥97% (SDS-PAGE)

form

powder

potency

0.02-0.3 ng/mL ED50/EC50

quality

endotoxin tested

mol wt

~17.4 kDa

packaging

pkg of 5x10 μg
pkg of 10 μg

storage condition

avoid repeated freeze/thaw cycles

technique(s)

cell culture | mammalian: suitable

impurities

<1 EU/μg

UniProt accession no.

storage temp.

−20°C

Gene Information

human ... TNF(7124)

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Application

TNF-α include stimulating growth of human fibroblasts and other cell lines activating polymorphonuclear neutrophils and osteoclasts and inducing interleukin-1, prostaglandin E2, and collagenase production.
Tumor Necrosis Factor-α (TNFα) human has been used:
  • to analyze the effects of cytokine TNFα-stressed human neuronal and glial (HNG) cells
  • to investigate the molecular mechanisms of TNFα-mediated prolyl-4 hydroxylase α1 (P4Hα1) suppression
  • to induce death-receptor-mediated apoptosis in HeLa cells.

Biochem/physiol Actions

Tumore necrosis factor-α (TNF-α), also known as cachectin, is expressed as a 26 kDa membrane bound protein and is then cleaved by TNF-α converting enzyme (TACE) to release the soluble 17 kDa monomer, which forms homotrimers in circulation. TNF-α plays roles in antitumor activity, immune modulation, inflammation, anorexia, cachexia, septic shock, viral replication and hematopoiesis. TNF-α is expressed by a great variety of cells, with numerous inductive and suppressive agents. Primarily, TNF-α is produced by macrophages in response to immunological challenges such as bacteria (lipopolysaccharides), viruses, parasites, mitogens and other cytokines. TNF-α is cytotoxic for many transformed cells (its namesake activity) but in normal diploid cells, it can stimulate proliferation (fibroblasts), differentiation (myeloid cells) or activation (neutrophils). TNF-α also shows antiviral effects against both DNA and RNA viruses and it induces production of several other cytokines. Although TNF-α is used in clinical trials as an antitumor agent, Sigma′s cytokine, growth factor and hormone products are for research only. TNF-α and the related molecule TNF-β (LT-α) share close structural homology with 28% amino acid sequence identity and both activate the same TNF receptors, TNFR1 and TNFR2. Mouse and human TNF-α share 79% amino acid sequence identity. Unlike human TNF-α, the mouse form is N-glycosylated.

Physical form

Lyophilized from a 0.2 μm-filtered buffer solution containing 3mM Tris-HCl and 5% trehalose.

Analysis Note

The biological activity of TNF-α is measured by the cytolysis of murine L929 cells.

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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A cytomegalovirus-encoded inhibitor of apoptosis that suppresses caspase-8 activation
Skaletskaya A, et al.
Proceedings of the National Academy of Sciences of the USA, 98(14), 7829-7834 (2001)
miRNA-155 up-regulation and complement factor H (CFH) deficits in Down?s Syndrome
Li YY, et al.
Neuroreport, 23(3), 168-168 (2012)
Role of NonO-histone interaction in TNFalpha-suppressed Prolyl-4-hydroxylase alpha1
Zhang C, et al.
Biochimica et Biophysica Acta - Molecular Cell Research, 1783(8), 1517-1528 (2008)
Casper Steenholdt et al.
The American journal of gastroenterology, 109(7), 1055-1064 (2014-05-07)
Cost-effective guidance of therapeutic strategy in Crohn's disease patients with secondary infliximab (IFX) treatment failure may be achieved by serum IFX and anti-IFX antibody (Ab) measurements by radioimmunoassay (RIA). This study investigated implications of using other techniques for this purpose.
David J Konieczkowski et al.
Cancer discovery, 4(7), 816-827 (2014-04-29)
Most melanomas harbor oncogenic BRAF(V600) mutations, which constitutively activate the MAPK pathway. Although MAPK pathway inhibitors show clinical benefit in BRAF(V600)-mutant melanoma, it remains incompletely understood why 10% to 20% of patients fail to respond. Here, we show that RAF

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