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Render Timestamp: 2024-12-26T11:29:07.183Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-11-19 23:03:09.650
Product last modified at: 2024-11-23T09:00:13.626Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
  1. Products /
  2. Primary Antibodies /
  3. GCDH (F2P2M) Rabbit mAb
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

GCDH (F2P2M) Rabbit mAb #43365

Filter:
  • WB
  • IHC
  • IF

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 48
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IHC-Immunohistochemistry 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunohistochemistry (Paraffin) 1:100 - 1:400
    Immunofluorescence (Immunocytochemistry) 1:50 - 1:200

    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

    GCDH (F2P2M) Rabbit mAb recognizes endogenous levels of total GCDH protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Trp50 of human GCDH protein.

    Background

    Glutaryl-CoA dehydrogenase (GCDH) is a mitochondria matrix enzyme that plays a role in the degradative pathway of lysine, hydroxylysine, and tryptophan by converting glutaryl-CoA to crotonyl-CoA (reviewed in 1). Crotonyl-CoA is further metabolized to acetyl-CoA, which enters the tricarboxylic acid (TCA) cycle for energy production. Mutation of the GCDH gene is the cause of glutamic aciduria type I (GAI), an autosomal recessive neurological disorder (2). GCDH deficiency leads to an accumulation of glutaryl-CoA and neurotoxic metabolites including glutaric acid and 3-hydroxyglutaric acid (3). Several studies have demonstrated the importance of GCDH in metabolic reprogramming in cancer. Melanoma cells can develop a dependency on GCDH (4). Mechanistically, loss of GCDH results in increased glutarylation of NRF2, a master transcriptional regulator of stress response genes associated with oxidative and metabolic stress responses, which results in increased NRF2 stability and activity and promotes cell death. Glioblastoma stem cells reprogram lysine catabolism, including upregulation of GCDH, which leads to an increase in histone crotonylation regulating tumor immunity (5). In contrast, in hepatocellular carcinoma (HCC), GCDH suppresses tumor growth and metastasis (6).

    Database Links

    UniProt ID: Q92947


    Entrez-Gene Id: 2639


    Limited Uses

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    For Research Use Only. Not For Use In Diagnostic Procedures.
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