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R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

GCLM (F7J2D) Rabbit mAb #33381

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  • WB
  • IP
  • IF

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 28
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:100
    Immunofluorescence (Frozen) 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

    GCLM (F7J2D) Rabbit mAb recognizes endogenous levels of total GCLM protein. Species reactivity by immunofluorescence is mouse only.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu212 of human GCLM protein.

    Background

    Glutamate-cysteine ligase modifier subunit (GCLM) is a component of the heterodimeric enzyme glutamate-cysteine ligase (GCL), which catalyzes the rate-limiting step in glutathione (GSH) biosynthesis, a ubiquitous intracellular peptide that plays vital roles in antioxidant defense, detoxification, cell proliferation, and other cellular functions (1,2). GCLM is one of a set of inhibitory ferroptosis genes that are normally repressed by the transcription factor BACH1 (a regulator in heme and iron metabolism) but are coordinately upregulated upon induction of ferroptosis with erastin (3). Additionally, when cells are starved for cysteine, the non-canonical activity of GCL can catalyze the synthesis of γ-glutamyl-peptide, therefore maintaining glutamate homeostasis to protect cells against ferroptosis (4).

    GCLM overexpression in bladder cancer is correlated with immune filtration and poor prognosis, and knockdown of GCLM can significantly suppress the colony formation ability of tumor cells, thus suggesting that GCLM is a potential therapeutic target (5). Indeed, in vitro treatment of BLCA cells with MTX-211, an EFGR and PI3K kinase inhibitor, promoted NFR2 degradation and subsequent downregulation of GCLM expression, resulting in decreased GSH levels and cell proliferation inhibition (6). Polymorphisms in the 5′ promoter region of GCLM are also associated with an increased risk of myocardial infarction (7), and GCLM may be implicated in other diseases where oxidative stress plays a significant role.
    For Research Use Only. Not For Use In Diagnostic Procedures.
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