Mouse Tumor Necrosis Factor-α (mTNF-α)

TNF-α, the prototypical member of the TNF protein superfamily, is a homotrimeric type-II membrane protein (1,2). Membrane bound TNF-α is cleaved by the metalloprotease TACE/ADAM17 to generate a soluble homotrimer (2). Both membrane and soluble forms of TNF-α are biologically active. TNF-α is produced by a variety of immune cells including T cells, B cells, NK cells and macrophages (1). Cellular response to TNF-α is mediated through interaction with receptors TNF-R1 and TNF-R2 and results in activation of pathways that favor both cell survival and apoptosis depending on the cell type and biological context. Activation of kinase pathways (including JNK, ERK (p44/42), p38 MAPK and NF-κB) promotes the survival of cells, while TNF-α mediated activation of caspase-8 leads to programmed cell death (1,2). TNF-α plays a key regulatory role in inflammation and host defense against bacterial infection, notably Mycobacterium tuberculosis (3).

Less than 0.01 ng endotoxin/1 μg mTNF-α.

>98% as determined by SDS-PAGE of 6 μg reduced (+) and non-reduced (-) recombinant mTNF-α. All lots are greater than 98% pure.

Recombinant mouse TNF-α (mTNF-α) Leu80-Leu235 (Accession #NP_038721) was expressed in human 293 cells at Cell Signaling Technology.

The bioactivity of recombinant mTNF-α was determined in a L-929 cell viability assay. The ED₅₀ of each lot is between 2-8 pg/ml.