Render Target: STATIC
Render Timestamp: 2024-12-09T11:52:10.709Z
Commit: 224419269841c11382c4555dbee545259bf6c379
XML generation date: 2024-08-01 15:31:18.835
Product last modified at: 2024-09-19T14:15:14.691Z
Cell Signaling Technology Logo
1% for the planet logo
PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

Phospho-RIP (Ser415) Antibody #88108

Filter:
  • WB

    Supporting Data

    REACTIVITY H M
    SENSITIVITY Endogenous
    MW (kDa) 78-82
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    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

    Phospho-RIP (Ser415) Antibody recognizes endogenous levels of mouse RIP protein only when phosphorylated at Ser415. This antibody can also detect human RIP protein when phosphorylated at Ser416.

    Species Reactivity:

    Human, Mouse

    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:

    Rat

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser415 of mouse RIP protein. Antibodies are purified by 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).

    Phosphorylation of mouse RIP at Ser415 (Ser416 in human) by AMPK in response to metabolic stress can inhibit RIP cell death (9).
    For Research Use Only. Not For Use In Diagnostic Procedures.
    Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.
    All other trademarks are the property of their respective owners. Visit our Trademark Information page.