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Merck

T6674

Sigma-Aldrich

Tumor Necrosis Factor-α human

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

Sinónimos:

hTNF-α, TNF-α

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About This Item

Número de CAS:
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.

Certificados de análisis (COA)

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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)
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)
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.
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Bacterial meningitis (BM) is an infectious disease that results in high mortality and morbidity. Despite efficacious antibiotic therapy, neurological sequelae are often observed in patients after disease. Currently, the main challenge in BM treatment is to develop adjuvant therapies that

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