Render Target: STATIC
Render Timestamp: 2024-10-09T11:05:31.464Z
Commit: f04ddd7fea9fb3592f59f61482fcb94610d25cbe
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

RIP4 Antibody #12636

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 86
    SOURCE Rabbit
    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 and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    RIP4 Antibody recognizes endogenous levels of total RIP4 protein.

    Species Reactivity:

    Human

    The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.

    Species predicted to react based on 100% sequence homology:

    Monkey

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human RIP4 protein. Antibodies are purified by protein A and peptide affinity chromatography.

    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).
    Receptor-interacting serine-threonine kinase 4 (RIP4, ANKRD3, DIK, PKK, or RIPK4) is a membrane-associated, ankyrin repeat-containing member of the RIP family first identified in HaCat cells (9,10). RIP4 has been shown to be involved in keratinocyte differentiation in vivo as well as wound repair (11-13). Studies indicate that siRNA knockdown of RIP4 in human xenografted tumor cells suppresses Wnt-dependent growth while over-expression of RIP4 in vitro stabilized β-catenin and lead to an increase in Wnt-dependent gene expression (14).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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