Render Target: STATIC
Render Timestamp: 2024-12-26T10:55:39.434Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-09-30 01:56:46.535
Product last modified at: 2024-12-17T19:02:52.178Z
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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.

SINTBAD (D1A5) Rabbit mAb #8605

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY
    SENSITIVITY Endogenous
    MW (kDa) 78-80
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 

    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, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    SINTBAD (D1D5) Rabbit mAb recognizes endogenous levels of total SINTBAD protein.

    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, Bovine

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu55 of human SINTBAD protein.

    Background

    SINTBAD, identified based on homology to NAP1, is an adaptor protein for TBK1 and IKKε, two related kinases that play a pivotal role in innate immune response (1). These kinases trigger the phosphorylation and subsequent activation of the transcription factor IRF-3, resulting in gene regulation required for immune responses (2). The precise mechanism by which SINTBAD activates TBK1 and IKKε is still unclear. Expression of a central region of SINTBAD termed a TBD (TBK binding domain) can function as a dominant negative protein and interfere with IRF-3 activation. SINTBAD and NAP1 can also bind to NDP52, a protein that associates with poly-ubiquitinated proteins, such as those produced on the surfaces of bacteria, and can trigger autophagy (3).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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