Render Target: SSR
Render Timestamp: 2024-11-14T23:07:18.820Z
Commit: 3c1f305a63297e594ac8d7bb5424007d592d68be
XML generation date: 2024-09-30 01:56:17.542
Product last modified at: 2024-11-13T20:00:09.914Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

TNF-α (D5G9) Rabbit mAb #6945

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 18, 25
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    TNF-α (D5G9) Rabbit mAb recognizes endogenous levels of total full length and secreted TNF-α protein. It can detect up to 10 pg of recombinant TNF-α by western blot.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with recombinant human TNF-α protein.

    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, Erk1/2, 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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