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Mouse Tumor Necrosis Factor-α (mTNF-α) #5178

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Inquiry Info. # 5178

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    Product Information

    Formulation

    With carrier: Lyophilized from a 0.22 μm filtered solution of PBS, pH 7.2 containing 20 μg BSA per 1 μg mTNF-α. Carrier free: Lyophilized from a 0.22 μm filtered solution of PBS, pH 7.2.

    Storage

    Stable in lyophilized state at -20°C for 1 year after receipt. Sterile stock solutions reconstituted with carrier protein are stable at 4°C for 2 months and at -20°C for 6 months. Avoid repeated freeze-thaw cycles.
    Maintain sterility. Storage at -20°C should be in a manual defrost freezer.

    Product Description

    MW (kDa) 16
    Purity >98% as determined by SDS-PAGE of 6 μg reduced (+) and non-reduced (-) recombinant mTNF-α. All lots are greater than 98% pure.
    Endotoxin Less than 0.01 ng endotoxin/1 μg mTNF-α.
    Activity 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.
    Molecular Formula Based on amino acid sequencing, greater than 50% of recombinant mTNF-α starts at Leu80 (LRSSS) and has a calculated MW of 17,257. The remainder starts at Ser82 (SSSQN). DTT-reduced and non-reduced protein migrate as 16 kDa polypeptides.

    Source / Purification

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

    Background

    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).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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