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  1. Products /
  2. Primary Antibodies /
  3. ALKBH5 (E5Y7C) Rabbit mAb
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Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

ALKBH5 (E5Y7C) Rabbit mAb #80283

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  • WB

    Supporting Data

    REACTIVITY H M R Mk
    SENSITIVITY Endogenous
    MW (kDa) 45-48
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 
    • Mk-Monkey 

    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

    ALKBH5 (E5Y7C) Rabbit mAb recognizes endogenous levels of total ALKBH5 protein. This antibody is predicted to detect all three ALKBH5 isoforms.

    Species Reactivity:

    Human, Mouse, Rat, Monkey

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly142 of human ALKBH5 protein.

    Background

    N6-methyladenosine (m6A) is an abundant and reversible RNA modification that plays an important role in mRNA splicing, processing, and stability. Demethylation of m6A is carried out by two enzymes, fat mass and obesity-related protein (FTO) and AlkB homolog 5 (ALKBH5). ALKBH5 belongs to the AlkB subfamily of Fe(II) and 2-oxoglutarate-dependent dioxygenases, and specifically recognizes the m6A modification within a conserved binding pocket (1). ALKBH5 knockout mice have been shown to be viable but harbor defects in spermatogenesis, primarily due to rampant apoptosis in spermatocytes (2). Specifically, ALKBH5 is required for late meiotic and haploid phases of spermatogenesis, and loss of m6A removal impairs mRNA splicing and stability necessary for the expression of key meiotic genes (3). ALKBH5 expression has been shown to be elevated in hypoxic models of breast cancer, resulting in increased m6A demethylation of NANOG mRNA and consequently promoting increased NANOG protein expression and accumulation of breast cancer stem cells (4). Knockdown of ALKBH5 has been shown to impair tumor formation in MDA-MB-231 breast cancer cells, and inhibition of ALKBH5 also represses tumorigenesis in glioblastoma stem-like cells (4,5). Interestingly, ALKBH5 may also show promise as a novel biomarker for pancreatic cancer, where increased expression was associated with higher overall survival rates (6).

    Database Links

    UniProt ID: Q6P6C2


    Entrez-Gene Id: 54890


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