Render Target: STATIC
Render Timestamp: 2024-11-22T10:57:09.538Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-09-30 01:57:32.262
Product last modified at: 2024-11-13T00:45:09.547Z
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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.

GCN2 (E7G7E) Rabbit mAb #65981

Filter:
  • WB
  • IP
  • IF

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 220
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:100
    Immunofluorescence (Immunocytochemistry) 1:6400 - 1:12800

    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

    GCN2 (E7G7E) Rabbit mAb recognizes endogenous levels of total GCN2 protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human GCN2 protein.

    Background

    Phosphorylation of the eukaryotic initiation factor 2 (eIF2) alpha subunit is a well-documented mechanism of downregulating protein synthesis under a variety of stress conditions. Kinases activated by viral infection (PKR), endoplasmic reticulum stress (PERK/PEK), amino acid deprivation (GCN2), and hemin deficiency (HRI) can phosphorylate the eIF2 alpha subunit (1,2). GCN2 is also required for UV light-induced translation inhibition, and in vivo phosphorylation of murine GCN2 at Thr898 is induced by both UV irradiation and by leucine deprivation (3). UV-induced activation of NF-κB also requires GCN2, which may act simply by preventing translation of IκB-alpha to replace pools that have been ubiquitinated and degraded (4). Interestingly, proteasome inhibitors (MG132 and ALLN) activate the GCN2/eIF2alpha pathway, suggesting a pivotal role for this kinase in stress response and ubiquitin-mediated signaling (5). In vitro autophosphorylation of yeast GCN2 within its activation loop at Thr882 and Thr887 (Thr898 and Thr903 in mouse) has also been reported (6).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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