Render Target: STATIC
Render Timestamp: 2024-12-20T11:56:31.595Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-12-17 23:02:08.163
Product last modified at: 2024-12-18T21:00:09.075Z
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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.

GRIM19 (F6I7Y) Rabbit mAb #76335

Filter:
  • WB

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 16
    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

    GRIM19 (F6I7Y) Rabbit mAb recognizes endogenous levels of total GRIM19 protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human GRIM19 protein.

    Background

    Gene associated with retinoic and interferon-induced mortality 19 (GRIM19), also known as nicotinamide adenine dinucleotide:ubiquinone oxidoreductase subunit A13 (NDUFA13), is a subunit of mitochondrial membrane complex I (1). GRIM19 expression is upregulated by IFN-β and retinoic acid, and in addition to its role in maintaining mitochondrial membrane potential, it antagonizes Stat3 to inhibit cell survival (1-3). In mouse models, due to its antagonism of Stat3, overexpression of GRIM19 has been shown to mitigate diet-induced obesity by promoting differentiation of adipocytes toward formation of brown adipose fat tissue rather than white adipose fat tissue (4). GRIM19 has also been found to act as a tumor suppressor and is downregulated in many cancers, including renal cell carcinoma, colon cancer, and several forms of lung cancer (5). In macrophages, GRIM19 knockdown was found to induce IL-1β secretion, enhance levels of NLRP3, caspase-1, and gasdermin D, and promote pyroptosis (6). Reduced GRIM19 levels were found in human chronic liver disease tissues, and deletion of GRIM19 in mouse liver elucidated a potential mechanism; deletion led to enhanced oxidative stress and NLRP3 activation, leading to hepatic fibrosis (7).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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