Render Target: STATIC
Render Timestamp: 2024-11-21T13:02:40.139Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-10-25 16:21:15.602
Product last modified at: 2024-11-14T13:15:44.308Z
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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.

PERK (D11A8) Rabbit mAb #5683

Filter:
  • WB
  • IP
  • IHC

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 140
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IHC-Immunohistochemistry 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50
    Immunohistochemistry (Paraffin) 1:1000 - 1:4000

    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

    PERK (D11A8) Rabbit mAb recognizes endogenous levels of total PERK protein. Staining of red blood cells has been observed. The specificity of this staining is unknown.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Trp164 of human PERK protein.

    Background

    Protein kinase-like endoplasmic reticulum kinase (PERK) is an eIF2α kinase and transmembrane protein resident in the endoplasmic reticulum (ER) membrane that couples ER stress signals to translation inhibition (1-3). ER stress increases the activity of PERK, which then phosphorylates eIF2α to promote reduced translation. Research studies have demonstrated that PERK-deficient mice have defects in pancreatic β cells several weeks after birth, suggesting a role for PERK-mediated translational control in protecting secretory cells from ER stress (4). PERK activation during ER stress correlates with autophosphorylation of its cytoplasmic kinase domain (1-3). Phosphorylation of PERK at Thr980 serves as a marker for its activation status.
    For Research Use Only. Not For Use In Diagnostic Procedures.
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