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CYB5R3 (F1D9O) Rabbit mAb #84402

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  • IF

    Supporting Data

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

    Product Information

    Product Usage Information

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

    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

    CYB5R3 (F1D9O) Rabbit mAb recognizes endogenous levels of total CYB5R3 protein.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro44 of human CYB5R3 protein.

    Background

    Cytochrome b5 reductase 3 (CYB5R3) is an essential flavoprotein that catalyzes the transfer of electrons from NADH to cytochrome b5. CYB5R3 is produced as two different isoforms: a membrane-bound form in somatic cells and a soluble form in erythrocytes (1). The membrane-bound form is found anchored primarily to the endoplasmic reticulum (ER) and is involved in desaturation and elongation of fatty acids, cholesterol biosynthesis, and drug metabolism. The soluble form functions in methemoglobin reduction and the regulation of aerobic metabolism (1). CYB5R3 has been shown to be a UFM1 substrate, with UFMylation being dependent on interactions with the E3 ligase components UFL1 and UFBP1. UFMylated CYB5R3 is converted to its inactive form and degraded in lysosomes, leading to the induction of ER-phagy (2).

    Mutations in the CYB5R3 gene can lead to both Type I and Type II methemoglobinemia, a rare genetic disorder characterized by elevated levels of methemoglobin in the blood, leading to chronic cyanosis and neurological dysfunction (3,4). Downregulation of CYB5R3 has been shown to promote tumorigenesis and lung metastasis in mouse models whereas overexpression can induce ER stress-mediated apoptosis, thus implicating CYB5R3 as a tumor suppressor (5). Additionally, CYB5R3 is essential for cardiomyocyte function and may have critical protective effects on vascular function and sudden cardiac death (6,7).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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