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Render Timestamp: 2024-11-14T22:31:52.655Z
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XML generation date: 2024-09-20 06:23:24.265
Product last modified at: 2024-09-25T12:15:14.891Z
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PDP - Template Name: Growth Factors and Cytokines
PDP - Template ID: *******9ad1159

Mouse TNF-α Recombinant Protein #24095

    Product Information

    Storage

    Mouse TNF-α Recombinant Protein is supplied as lyophilized material that is very stable at -20°C. It is recommended to reconstitute with sterile water at a concentration of 0.1 mg/mL which can be further diluted in aqueous solutions as needed. Addition of a carrier protein (0.1% HSA or BSA) is recommended for long-term storage.

    Once in solution, store at 4°C and use within 1 month, or store at -20ºC to -80ºC and use within 3 months to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles if storing reconstituted material at -20ºC to -80ºC.

    Product Description

    MW (kDa) 17.4
    Purity A greater than or equal to 95% purity was determined by SDS-PAGE.
    Endotoxin Endotoxin levels are less than or equal to 1 EU / 1 μg mTNF-α.
    Activity The bioactivity of recombinant mTNF-α was determined in a cell proliferation assay measuring the cytolysis of mouse L929 cells in the presence of Actinomycin D. The ED50 of each lot is less than or equal to 100 pg/mL.

    Source / Purification

    Recombinant mouse TNF-α was expressed in E. coli and is supplied in a lyophilized form.

    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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