Acetyl-p53 (Lys382) Antibody [K2J24]

Catalog No.: F2232

For research use only.

    Home Primary Antibodies Acetyl-p53 (Lys382) Antibody [K2J24]

    Application: Reactivity:

    Usage Information

    Dilution
    1:250 - 1:5000
    1:100 - 1:250
    1:20
    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
    53 kDa

    Datasheet & SDS

    Biological Description

    Specificity
    Acetyl-p53 (Lys382) Antibody [K2J24] detects endogenous levels of p53 only when acetylated at lysine 382.
    Clone
    K2J24
    Synonym(s)
    P53; TP53; Cellular tumor antigen p53; Antigen NY-CO-13; Phosphoprotein p53; Tumor suppressor p53
    Background
    Acetyl-p53 (Lys382) refers to the tumor suppressor protein p53 that has undergone acetylation at its conserved carboxyl-terminal lysine 382, a key post-translational modification regulating its stability and activity. Structurally, p53 is a 393-amino acid transcription factor composed of an N-terminal transactivation domain, a central DNA-binding domain, an oligomerization domain, and a C-terminal regulatory domain where Lys382 resides. Acetylation at Lys382, mediated mainly by histone acetyltransferases such as p300/CBP and PCAF, enhances p53’s DNA-binding affinity, prevents MDM2-mediated degradation, and promotes its accumulation in the nucleus. Acetyl-p53 (Lys382) is widely expressed in mammalian cells but its levels are tightly controlled and increase under stress conditions such as DNA damage, oxidative stress, or treatment with histone deacetylase inhibitors (HDACi). Functionally, acetylation at Lys382 not only augments the transcriptional activity of p53 in driving the expression of cell cycle regulators (e.g., p21) and proapoptotic genes (e.g., BAX, PUMA, DR5), but also facilitates its transcription-independent roles at mitochondria. Specifically, Lys382 acetylation enables p53 to disrupt the inhibitory Ku70-BAX complex, thereby freeing BAX to translocate to mitochondria, generate reactive oxygen species, and promote apoptosis. Thus, Acetyl-p53 (Lys382) represents a critical molecular switch integrating stress responses, tumor suppression, and apoptosis.
    References
    • https://pubmed.ncbi.nlm.nih.gov/19265193/

    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.

    * Indicates a Required Field

    Please enter your name.
    Please enter your email. Please enter a valid email address.
    Please write something to us.