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Render Timestamp: 2024-11-21T13:40:13.902Z
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XML generation date: 2024-10-30 15:02:10.474
Product last modified at: 2024-10-31T07:00:54.955Z
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PDP - Template Name: Antibody Sampler Kit
PDP - Template ID: *******4a3ef3a

Toll-like Receptor Antibody Sampler Kit #9971

    Product Information

    Product Description

    The Toll-Like Receptor Antibody Sampler Kit is an economical way to examine the total protein levels of a number of toll-like receptors. This kit includes enough primary and secondary antibodies to perform two Western blot experiments with each antibody.

    Specificity / Sensitivity

    All antibodies contained in this kit detect endogenous levels of their respective total TLR protein. Cross reactivity was not detected with other family members at physiological conditions.

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide and are purified by protein A and peptide affinity chromatography. Monoclonal antibodies are produced by immunizing animals with recombinant human proteins or synthetic peptides.

    Background

    Members of the Toll-like receptor (TLR) family, named for the closely related Toll receptor in Drosophila, play a pivotal role in innate immune responses (1-4). TLRs recognize conserved motifs found in various pathogens and mediate defense responses (5-7). Triggering of the TLR pathway leads to the activation of NF-κB and subsequent regulation of immune and inflammatory genes (4). The TLRs and members of the IL-1 receptor family share a conserved stretch of approximately 200 amino acids known as the Toll/Interleukin-1 receptor (TIR) domain (1). Upon activation, TLRs associate with a number of cytoplasmic adapter proteins containing TIR domains, including myeloid differentiation factor 88 (MyD88), MyD88-adapter-like/TIR-associated protein (MAL/TIRAP), TIR domain-containing adapter-inducing IFN-β (TRIF), and Toll-receptor-associated molecule (TRAM) (8-10). This association leads to the recruitment and activation of IRAK1 and IRAK4, which form a complex with TRAF6 to activate TAK1 and IKK (8,11-14). Activation of IKK leads to the degradation of IκB, which normally maintains NF-κB in an inactive state by sequestering it in the cytoplasm.
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