Home Primary Antibodies Acetyl-p53 (Lys373) Antibody [J7D9]

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Acetyl-p53 (Lys373) Antibody [J7D9]

Catalog No.: F2048

    Application: Reactivity:
    • F2048-wb
      Lane 1: HepG2, Lane 2: HepG2 (etoposide, 30 ug/mL, 8 h; trichostatin A, 500 ng/mL, 4 h)

    Usage Information

    Dilution
    1:5000
    1:100 - 1:250
    1:120
    Application
    WB, IF, FCM
    Reactivity
    Human
    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 Observed MW
    43 kDa 53 kDa
    *Why do the predicted and actual molecular weights differ?
    The following reasons may explain differences between the predicted and actual protein molecular weight.

    Datasheet & SDS

    Biological Description

    Specificity
    Acetyl-p53 (Lys373) Antibody [J7D9] detects endogenous levels of total p53 protein only when it is Acetylated at Lys373.
    Clone
    J7D9
    Synonym(s)
    P53; TP53; Cellular tumor antigen p53; Antigen NY-CO-13; Phosphoprotein p53; Tumor suppressor p53
    Background
    Acetyl-p53 (Lys373) refers to the post-translationally modified form of the p53 tumor suppressor protein, a sequence-specific DNA-binding transcription factor belonging to the p53 family that regulates genes involved in cell cycle arrest, DNA repair, senescence, and apoptosis. p53 features an N-terminal transactivation domain (TAD), a central DNA-binding domain containing key residues like K120, and a C-terminal regulatory domain with multiple lysine sites, including K373 (often studied alongside K382), that undergo acetylation by histone acetyltransferases such as p300/CBP, which neutralizes their positive charge to promote an open conformation and enhance DNA binding affinity. Acetylation at K373/K382 stabilizes p53 by reducing ubiquitination and degradation, recruits p300 to promoters like that of p21^Waf1/Cip1, and boosts transcriptional activation of cell cycle inhibitors independent of N-terminal phosphorylation (e.g., Ser15, Ser20, Ser392), thereby inducing p21 expression, G1/S arrest, and tumor suppression while responding to HDAC inhibitors like depsipeptide. This modification fine-tunes p53's pathway choices, favoring growth arrest over apoptosis in certain contexts such as DNA damage or genotoxic stress, with disease relevance in cancer, where its dysregulation promotes proliferation.
    References
    • https://pubmed.ncbi.nlm.nih.gov/16537920/
    • https://pubmed.ncbi.nlm.nih.gov/25545885/

    Tech Support

    Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

    Handling Instructions

    Tel: +1-832-582-8158 Ext:3
    If you have any other enquiries, please leave a message.

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