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654245

Sigma-Aldrich

TNF-α, Mouse, Recombinant, E. coli

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Synonym(s):
rmTNF-α, rm-Cachectin, Tumor Necrosis Factor-α
UNSPSC Code:
12352202
NACRES:
NA.32

Assay

≥97% (SDS-PAGE)

Quality Level

form

lyophilized

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze

impurities

≤100 pg/μg Endotoxin (pg/μg TNF-α)

shipped in

ambient

storage temp.

−70°C

General description

Reasearch area: Apoptosis

Recombinant mouse tumor necrosis factor-α (TNF-α), expressed in E. coli, is known for its direct tumoricidal capabilities. This inflammatory cytokine triggers a cascade of other cytokines and factors constituting the immune system′s response to infections and cancer. Additionally, it has been reported to influence changes in bone metabolism during inflammation. (TNF-α), a homotrimer protein, occurs in a soluble and transmembrane form.

Application

TNF-α, Mouse, Recombinant, E. coli has been used to study TNF-signaling to insulin gene expression in insulin-producing cells.

Biochem/physiol Actions

TNF-α, a cytokine, interacts with two distinct receptors, initiating signal transduction pathways that result in cellular responses, such as cell survival, differentiation, and proliferation. It regulates inflammatory responses and activates inflammatory molecules, including other cytokines and chemokines. Transmembrane TNF-α binds to TNFR1 and TNFR2 and facilitates inflammation and cell death. However, excessive or inappropriate activation of TNF-α signaling is linked to chronic inflammation and may lead to pathological complications, including autoimmune diseases. Rheumatoid arthritis (RA), inflammatory bowel disease (IBD), psoriatic arthritis (PsA), psoriasis (PS), and noninfectious uveitis (NIU) are few conditions.

Additionally, TNF-α is associated with insulin signaling inhibition. Its removal ameliorates insulin sensitivity. The activity of the Jun N-terminal kinase (JNK) signaling pathway, which is abnormally elevated in obesity, is strongly activated by both TNF-α.

ED₅₀ = 20-50 pg/ml as measured in a cytotoxic assay using the TNF-α susceptible murine L-929 cell line in the presence of Actinomycin D (Cat. No. 114666)

Warning

Toxicity: Standard Handling (A)

Physical form

Lyophilized from sterile-filtered PBS, 50 µg BSA/µg TNF-α.

Reconstitution

Following reconstitution, aliquot and freeze (-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 1 month at 4°C or for up to 3 months at -70°C.
Reconstitute to a concentration ≥10 µg/ml with sterile PBS containing ≥0.1% HSA or BSA.

Other Notes

Scharla, S.H., et al. 1994. Eur. J. Endocrinol. 131, 293.
Eck, M.J., et al. 1992. J. Biol. Chem. 267, 2119.

Legal Information

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

WGK

WGK 1

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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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, 22(5)-22(5) (2021)
Adilson Guilherme et al.
The Journal of biological chemistry, 284(25), 17082-17091 (2009-03-27)
The nuclear receptor peroxisome proliferator-activated receptor gamma (PPARgamma) is a ligand-dependent transcription factor that acts as a primary regulator of adipogenesis and controls adipocyte metabolism and insulin action. Increased expression of tumor necrosis factor (TNFalpha) in adipose tissue of obese
Xuyong Chen et al.
The Journal of clinical investigation, 130(12), 6443-6456 (2020-08-19)
Interstitial cells of Cajal (ICCs) are pacemaker cells in the intestine, and their function can be compromised by loss of C-KIT expression. Macrophage activation has been identified in intestine affected by Hirschsprung disease-associated enterocolitis (HAEC). In this study, we examined
Overexpression of II?Ba?? modulates NF-I?B activation of inflammatory target gene expression.
Downton, et al.
Frontiers in molecular biosciences, 10, 1187187-1187187 (2023)

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