Tumor Necrosis Factor-α from rat

The Tnf (tumor necrosis factor) gene is mapped to rat chromosome 20p12.

TNF-α influences the growth and function of both normal and neoplastic cells. TNF-α causes cytolysis or cytostasis of certain transformed cells being synergistic with γ-interferon in its cytotoxicity.

Tumor Necrosis Factor-α from rat has been used:

• To stimulate inducible nitric oxide synthase (iNOS) expression in the macrophages as an indication of M1 macrophage activation
• To study its effect on pancreatic β cell apoptosis
• To evaluate the effect of progesterone on the expression of tumor necrosis factor (TNF)-α in synovial membrane
• As a blocking antigen in the control, for immunohistochemical analysis

Tumor necrosis factor-α (TNF-α), also known as cachectin, plays roles in antitumor activity, immune modulation, inflammation, anorexia, cachexia, septic shock, viral replication, and hematopoiesis. TNF-α is expressed by a variety of cells, with numerous inductive and suppressive agents. It is primarily 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. 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.

Lyophilized from an 0.2 μm-filtered buffered solution with bovine serum albumin as a carrier.

The biological activity is measured in a cytotoxic assay using a TNF-susceptible mouse L929 cell line in the presence of actinomycin D.