Render Target: STATIC
Render Timestamp: 2024-09-17T09:41:02.740Z
Commit: 195d6e018d1f29a59e5c111fed767382e8d7f01b
1% for the planet logo
PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

BLVRA (F7Z7R) Rabbit mAb #38276

Filter:
  • WB
  • IHC

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 38
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IHC-Immunohistochemistry 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunohistochemistry (Paraffin) 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

    BLVRA (F7Z7R) Rabbit mAb recognizes endogenous levels of total BLVRA protein. This antibody detects a 120 kDa band of unknown origin in some cell lines. Non-specific staining was observed in human skeletal muscle by immunohistochemistry.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly91 of human BLVRA protein.

    Background

    Biliverdin reductase A (BLVRA or BVRA) is responsible for the reduction of biliverdin, a product of heme oxygenase, to produce bilirubin, the end product of the heme catabolic pathway and major physiological antioxidant (1). In addition to its canonical role as an antioxidant, bilirubin acts as a powerful immunosuppressant and has hormonal activity that links it to a number of signaling pathways (reviewed in 2-4). Altered levels of bilirubin and BVRA have been reported in many pathological conditions, including cancer, cardiovascular, metabolic, and neurodegenerative diseases. Deletion of BLVRA leads to an increase in oxidative stress and autophagy impairment (5,6). BVRA has been shown to be a substrate of the insulin receptor and also phosphorylates insulin receptor substrate 1 (IRS-1) to regulate the insulin signaling pathway (7). Reduced BVRA expression is associated with changes in insulin signaling during obesity (8). BVRA phosphorylation of glycogen synthase kinase-3β (GSK-3β) inhibits its activity and phosphorylation of peroxisome proliferator-activated receptor α (PPARα), which protects from hepatic steatosis (9). Impairment of BVRA has been associated with Alzheimer’s disease (10-12). Levels of BVRA are frequently elevated in cancer, where it regulates several key mitogenic pathways (reviewed in 13).
    1. Komuro, A. et al. (1996) Biochim Biophys Acta 1309, 89-99.
    2. Vitek, L. et al. (2023) Trends Mol Med 29, 315-328.
    3. Creeden, J.F. et al. (2021) Am J Physiol Endocrinol Metab 320, E191-E207.
    4. Kapitulnik, J. and Maines, M.D. (2009) Trends Pharmacol Sci 30, 129-37.
    5. Gordon, D.M. et al. (2019) Arch Biochem Biophys 672, 108072.
    6. Lanzillotta, C. et al. (2020) Antioxidants (Basel) 9, 671. doi: 10.3390/antiox9080671.
    7. Lerner-Marmarosh, N. et al. (2005) Proc Natl Acad Sci USA 102, 7109-14.
    8. Cimini, F.A. et al. (2019) Biochim Biophys Acta Mol Basis Dis 1865, 1490-1501.
    9. Hinds, T.D. et al. (2016) J Biol Chem 291, 25179-25191.
    10. Sharma, N. et al. (2019) Neurobiol Dis 125, 176-189.
    11. Barone, E. et al. (2019) Mol Neurobiol 56, 2922-2943.
    12. Triani, F. et al. (2018) Biochim Biophys Acta Mol Basis Dis 1864, 3181-3194.
    13. Gibbs, P.E. et al. (2015) Front Pharmacol 6, 119.
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