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Acetyl-β Catenin (Lys49) Antibody [N20A14]

Cat.No.: F8516

    Application: Reactivity:

    Usage Information

    Dilution
    1:1000
    1:200
    Application
    WB, IP
    Reactivity
    Human, Mouse, Monkey
    Source
    Rabbit Monoclonal Antibody
    Storage Buffer
    PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
    Storage (from the date of receipt)
    -20°C (avoid freeze-thaw cycles), 2 years
    Predicted MW
    92 kDa
    Positive Control SW480 cells; SW620 cells; COLO 205 cells
    Negative Control HeLa cells; MCF7 cells

    Datasheet & SDS

    Biological Description

    Specificity
    Acetyl-β Catenin (Lys49) Antibody [N20A14] detects endogenous levels of total β Catenin protein only when it is Acetylated at Lys49.
    Clone
    N20A14
    Synonym(s)
    Catenin beta-1; Beta-catenin; CTNNB1; CTNNB
    Background
    Acetyl-β-Catenin Lys49 is a post-translationally modified form of β-catenin, a central effector of Wnt signaling and a key scaffold at cadherin-based cell junctions. Acetylation at Lys49, located within the N-terminal unstructured domain, is mediated by CBP and PCAF acetyltransferases and modulates both protein stability and subcellular localization. Lys49 lies adjacent to the GSK3β and CK1 phosphorylation sites in the first armadillo repeat flank; acetylation at this site neutralizes its positive charge and physically blocks recognition by the β-TrCP E3 ubiquitin ligase, preventing ubiquitination and subsequent proteasomal degradation. This modification primarily competes with ubiquitination at Lys49 and nearby Lys19, thereby stabilizing β-catenin in the cytoplasm, promoting its nuclear translocation, and enhancing the activation of Wnt target genes such as c-Myc and Cyclin D1. Additionally, acetylation at Lys49 facilitates β-catenin’s recruitment to adherens junctions by promoting its interaction with E-cadherin, which strengthens actin cytoskeleton anchorage and cell-cell adhesion. This regulatory mechanism supports Wnt-driven proliferation and epithelial-mesenchymal transition during development and tumorigenesis. Mutations or hypermethylation of Lys49 are observed in anaplastic thyroid carcinoma, while HDAC6-mediated deacetylation at this residue leads to cytosolic degradation of β-catenin and synaptic deficits in neural progenitors.
    References
    • https://pubmed.ncbi.nlm.nih.gov/11973335/
    • https://pubmed.ncbi.nlm.nih.gov/32355204/

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