Render Target: STATIC
Render Timestamp: 2024-11-22T12:04:38.821Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-11-14 23:10:25.524
Product last modified at: 2024-11-15T09:00:39.373Z
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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.

RIP3 (E1Y9Z) Rabbit mAb (BSA and Azide Free) #91171

Filter:
  • ELISA

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa)
    Source/Isotype Rabbit IgG
    Application Key:
    • ELISA-ELISA 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN or CUT&Tag assays. If you require a carrier free formulation for chromatin profiling, please contact us. Optimal dilutions/concentrations should be determined by the end user.

    BSA and Azide Free antibodies are quality control tested by size exclusion chromatography (SEC) to determine antibody integrity.

    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 -20°C. This product will freeze at -20°C 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.

    Specificity / Sensitivity

    RIP3 (E1Y9Z) Rabbit mAb (BSA and Azide Free) detects endogenous levels of RIP3.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with synthetic peptide corresponding to residues in human RIP3.

    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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