Render Target: SSR
Render Timestamp: 2024-10-24T19:56:21.877Z
Commit: 56767fe525c928647c8401233a175d0d607d385d
XML generation date: 2024-10-22 16:01:07.490
Product last modified at: 2024-10-22T07:01:01.123Z
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PDP - Template Name: Matched Antibody Pair
PDP - Template ID: *******446e1e7

Total RIP3 Matched Antibody Pair #71588

Filter:
  • ELISA

    Supporting Data

    REACTIVITY M R
    Application Key:
    • ELISA-ELISA 
    Species Cross-Reactivity Key:
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Matched Antibody Pairs include capture and detection antibodies to non-overlapping epitopes. Optimal dilutions/concentrations should be determined by the end user.

    Formulation

    Supplied in 1X PBS (10 mM Na2HPO4, 3 mM KCl, 2 mM KH2PO4, and 140 mM NaCl (pH 7.8)). BSA and Azide Free.

    Storage

    Store at -20ºC. This product will freeze at -20ºC so it is recommended to aliquot into single-use vials to avoid multiple freeze/thaw cycles. A slight precipitate may be present and can be dissolved by gently vortexing. This will not interfere with antibody performance.

    Product Description

    The Total RIP3 Matched Antibody Pair is ideal for use with immunoassay technologies and high-throughput ELISA platforms requiring antibody pairs with specialized or custom antibody labeling. Labels include fluorophores, lanthanides, biotin, and beads. Platforms requiring conjugated Matched Antibody Pairs include MSD, Quanterix Simoa, Alpha Technology (AlphaScreen, AlphaLISA, LANCE, HTRF), and Luminex.

    Learn how Matched Antibody Pairs move your projects forward, faster at cst-science.com/matched-antibody-pairs.

    Background

    The receptor-interacting protein (RIP) family of serine-threonine kinases (RIP, RIP2, RIP3, and RIP4) are important regulators of cellular stress that trigger pro-survival and inflammatory responses through the activation of NF-κB, as well as pro-apoptotic pathways (1). In addition to the kinase domain, RIP contains a death domain responsible for interaction with the death domain receptor Fas and recruitment to TNF-R1 through interaction with TRADD (2,3). RIP-deficient cells show a failure in TNF-mediated NF-κB activation, making the cells more sensitive to apoptosis (4,5). RIP also interacts with TNF-receptor-associated factors (TRAFs) and can recruit IKKs to the TNF-R1 signaling complex via interaction with NEMO, leading to IκB phosphorylation and degradation (6,7). Overexpression of RIP induces both NF-κB activation and apoptosis (2,3). Caspase-8-dependent cleavage of the RIP death domain can trigger the apoptotic activity of RIP (8).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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