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Render Timestamp: 2024-10-09T10:29:04.469Z
Commit: f04ddd7fea9fb3592f59f61482fcb94610d25cbe
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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.

Phospho-Tyk2 (Tyr1054/1055) (D7T8A) Rabbit mAb #68790

Filter:
  • WB

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 134
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 

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

    Protocol

    Specificity / Sensitivity

    Phospho-Tyk2 (Tyr1054/1055) (D7T8A) Rabbit mAb recognizes endogenous levels of Tyk2 protein only when phosphorylated at Tyr1054 and Tyr1055. Cross-reactivity was not observed with other Jak family members.

    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:

    Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic phospho-peptide corresponding to residues surrounding Tyr1054/1055 of human Tyk2 protein.

    Background

    Tyk2 is a member of the Jak family of protein tyrosine kinases. It associates with and is activated by receptors for many cytokines including IL-13, the IL-6 family, IL-10, and IFN-α and β (1-3). Following ligand binding, Tyk2 is activated by phosphorylation of Tyr1054 and/or Tyr1055 (4). Tyk2 is required for the tyrosine phosphorylation of Stat3 in the IFN-β signaling cascade (5).
    The role of Tyk2 has been extensively studied in terms of its involvement in immune regulation and pathological significance (reviewed in 6). Deletion of Tyk2 in mice results in increased sensitivity to infection and defective tumor surveillance, but only a partial effect on Type I interferon signaling (7, 8). In contrast, a human patient diagnosed with hyper-IgE syndrome having increased susceptibility to various microorganisms was found to have a homozygous mutation of Tyk2 (9). These studies suggest a more critical role of Tyk2 in humans with regards to Type I interferon signaling as well as other cytokines including IL-23, IL-6, and IL-10.
    For Research Use Only. Not For Use In Diagnostic Procedures.
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