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Key Documents

654205-M

Sigma-Aldrich

TNF-α, Human, Recombinant, E. coli

Synonym(s):

TNF-α, Human, Recombinant, E. coli, rhTNF-α, rh-Cachectin, Tumor Necrosis Factor-α

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About This Item

CAS Number:
MDL number:
UNSPSC Code:
12352202
NACRES:
NA.27

biological source

human

Quality Level

recombinant

expressed in E. coli

Assay

≥95% (SDS-PAGE)

form

lyophilized

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze

impurities

≤0.1 ng/μg Endotoxin (ng/μg TNF-α)

solubility

distilled water: 0.1—1 mg/mL

storage temp.

−70°C

Gene Information

human ... TNF(7124)

General description

Research area: Apoptosis
Tumor Necrosis Factor alpha (TNF α), a homotrimer protein made of 157 amino acids, is produced by macrophages/monocytes, T-lymphocytes, and natural killer cells during acute inflammation. soluble and transmembrane form. The precursor form of TNF-α is in transmembrane form (tmTNF-α), which is processed to release soluble form (sTNF-α).

Application

TNF-α, Human, Recombinant, E. coli has been used to stimulate NF-κB activation and study the effects of pancreatic elastase on cellular responses.

Biochem/physiol Actions

Recombinant, human tumor necrosis factor-α expressed in E. coli., a cytokine produced primarily by activated macrophages, activates a variety of immune defense mechanisms by interactions with polymorphonuclear leukocytes, T cells, antibody-producing B lymphocytes, fibroblasts, and hematopoietic bone marrow cells. Activity is not species-specific. Induces apoptosis in human blood and bone marrow neutrophils and in endothelial cells. Increases the iNOS levels in vascular smooth muscle cells. Involved in pathophysiological processes of several chronic and acute diseases. Stimulates stress-activated protein kinase (SAPK). ED₅₀ = 20-50 pg/ml as measured in a cytotoxicity assay with the TNF-α-susceptible murine L-929 cell line in the presence of Actinomycin D (Cat. No. 114666)
Tumor Necrosis Factor alpha (TNF alpha), is an inflammatory cytokine. It coordinates a range of signaling events within cells, leading to necrosis or apoptosis. TNF-α initiates signal transduction pathways by binding to TNFR-1 and TNFR-2. These pathways cause cellular processes such as cell survival, differentiation, and proliferation.

Warning

Toxicity: Standard Handling (A)

Reconstitution

Following reconstitution, aliquot and freeze (-20°C or -70°C) for long-term storage or refrigerate (4°C) for short-term storage. Avoid freeze/thaw cycles of solutions. Stock solutions are stable for up to 3 months at -20°C or -70°C or up to 1 month at 4°C.
Reconstitute with sterile, dH₂O to a final concentration of 0.1-1 mg/ml. Further dilutions should be made in low endotoxin medium or aqueous buffer containing carrier protein such as heat inactivated FCS or tissue culture grade BSA.

Other Notes

Merck Index 13, 9882.
Tsuchida, H., et al. 1995. J. Immunol. 154, 2403.
Westwick, J.K., et al. 1995. J. Biol. Chem. 270, 22689.
Polunovsky, V.A., et al. 1994. Exp. Cell Res.214, 584.
Koide, M., et al. 1993. FEBS Lett.318, 213.
Vilcek, J., and Lee, T.H. 1991. J. Biol. Chem.266, 7313.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Storage Class Code

12 - Non Combustible Liquids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

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H T Idriss et al.
Microscopy research and technique, 50(3), 184-195 (2000-07-13)
Tumour Necrosis Factor alpha (TNF alpha), is an inflammatory cytokine produced by macrophages/monocytes during acute inflammation and is responsible for a diverse range of signalling events within cells, leading to necrosis or apoptosis. The protein is also important for resistance
The Role of Tumor Necrosis Factor Alpha (TNF-?) in Autoimmune Disease and Current TNF-? Inhibitors in Therapeutics
Dan-in Jang, et al.
International Journal of Molecular Sciences (2021)
Antti Hietaranta et al.
Biochemical and biophysical research communications, 323(1), 192-196 (2004-09-08)
Pancreatic elastase has been implicated in the pathophysiology of severe acute pancreatitis, characterized by systemic inflammatory response, distant organ failure, and high mortality. Here we show that pancreatic elastase activates transcription factors NF-kappaB, AP-1, and NFAT in human myeloid cells

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