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Tumor Necrosis Factor

human, recombinant, E. coli

Product Cat. No. Amount Price (EUR) Buy / Note
TNF α PR-430 50 μg 207,00 Add to Basket/Quote Add to Notepad

For in vitro use only!

Shipping: shipped on dry ice

Storage Conditions: store at -80 °C
avoid freeze/thaw cycles

Shelf Life: 12 months

Accession number: U42625

Accession number: U42625

Purity: > 95 % (SDS-PAGE)

Form: liquid (Supplied in 20 mM Tris-HCl pH 8.0, 5 mM MgCl2, 10% glycerol and BSA as carrier)

pH: 8.0

Activity: 2x108 units/mg

Tumor Necrosis Factor α (TNFα), named for its antitumour properties, is a vital member of the multifunctional TNF superfamily and has important roles in immunity and cellular remodelling as well as influencing apoptosis and cell survival. Its central role in inflammation has led to the development of TNFα antagonists as effective therapies for rheumatoid arthritis and inflammatory bowel disease. It is known that TNFα is a crucial cytokine in the establishment an maintenance of inflammation in multiple autoimmune diseases. In addition to its established role in the immune system, TNFα exerts complex regulatory actions on adipose tissue. TNFα affects many aspects of adipocyte function, from adipocyte development to lipid metabolism.

Selected References:
Meager et al. (1987) Quantification of interferons by anti-viral assays and their standardization. Lymphokines and Interferons-A Practical Approach. IRL, Oxford:129.
Roilides et al. (2003) Immunomodulation of invasive fungal infections. Infectious Disease Clinics of North America 16:193.
Reimold (2002) TNFalpha as therapeutic target: new drugs, more applications. Curr. Drug Targets Inflamm. Allergy 1:377.
Szlosarek et al. (2003) Tumor necrosis factor alpha: a potential target for the therapy of solid tumours. Lancet Oncol. 4:565.
Warne (2003) Tumor necrosis factor alpha: a key regulator of adipose tissue mass. J. Endocrinol. 177:351.
Agnello et al. (2003) Cytokines and transcription factors that regulate T helper cell differentiation: New players and new insights. Journal of Clinical Immunology 23:147.
Ohba et al. (2011) Identification of interleukin-1 receptor-associated kinase 1 as a critical component that induces post-transcriptional activation of IκB-Zeta. The FEBS Journal 279 (2):211.