Acetyl-p53-K382 Rabbit Polyclonal Antibody (P04637) for Dot Blot and ELISA

Core Product Specifications and Parameters

Biological Background: Cellular Tumor Antigen p53 (TP53) Function and Localization

Cellular tumor antigen p53 (TP53) is a multifunctional transcription factor that plays a central role in tumor suppression by inducing cell cycle arrest, DNA repair, or apoptosis in response to cellular stress. It acts as a guardian of the genome, negatively regulating cell division by controlling the expression of key target genes, including inhibitors of cyclin-dependent kinases. p53-mediated apoptosis involves stimulation of BAX and FAS antigen expression or repression of Bcl-2, and its pro-apoptotic activity is modulated by interactions with ASPP family proteins. Additionally, p53 regulates the circadian clock by repressing CLOCK-BMAL1-mediated transcription of PER2. Related references: PMID:11025664, PMID:12524540, PMID:12810724, PMID:15340061, PMID:24051492

p53 localizes to multiple subcellular compartments depending on its activation state and isoform. It is predominantly nuclear, but can be found in the cytoplasm, at PML nuclear bodies, mitochondria, the endoplasmic reticulum, and the centrosome. Translocation to mitochondria occurs under oxidative stress or mitomycin C treatment, where p53 cooperates with PPIF to activate necrosis. Related references: PMID:15340061, PMID:17170702, PMID:11025664, PMID:12810724, PMID:22726440, PMID:27323408, PMID:28842590

p53 is ubiquitously expressed, but its isoforms show tissue‑dependent variation. Isoform 2 is absent in brain, lung, and prostate, while isoform 8 is limited to colon, bone marrow, testis, fetal brain, and intestine. Related references: PMID:16131611

p53 undergoes extensive post‑translational modifications that regulate its stability and activity. Acetylation at lysine 382 (K382) is mediated by acetyltransferases such as p300/CBP and enhances p53 DNA binding and transcriptional activation. This modification can be reversed by deacetylases, and K382 can also be methylated or dimethylated, highlighting a complex regulatory network. Related references: PMID:10656795, PMID:15448695, PMID:20228809, PMID:23431171, PMID:29681526, PMID:19608861, PMID:17707234, PMID:20870725, PMID:22864287

Experimental Guidance and Technical Tips

• The immunogen is a synthetic acetylated peptide corresponding to residues around K382 of human p53. The antibody is expected to specifically recognize the acetylated form; cross‑reactivity with unmodified peptide or other modifications at this site should be tested.
• For dot blot applications, consider using denatured protein samples or peptides spotted onto membranes. For ELISA, coating with the immunogen peptide or full‑length p53 protein may be suitable.
• Because polyclonal antibodies can exhibit batch‑to‑batch variation, validate the antibody’s specificity in your experimental system using appropriate controls (e.g., non‑acetylated peptide competition, or lysates from cells treated with deacetylase inhibitors like trichostatin A).
• Induction of p53 acetylation can be achieved by treating cells with DNA‑damaging agents (e.g., doxorubicin, etoposide) prior to sample preparation.
• The antibody is shipped on ice bags. Upon receipt, aliquot and store at –20°C or lower for long‑term stability. Avoid repeated freeze‑thaw cycles.

CamelBio: Your One-Stop Sourcing Bridge

CamelBio serves as a comprehensive one‑stop sourcing partner for IVD raw materials, offering diagnostic manufacturers, laboratories, and research institutions streamlined access to a vast portfolio of antibodies, antigens, and ancillary reagents. This Acetyl‑p53‑K382 Rabbit pAb targets a critical post‑translational modification of the tumor suppressor p53, making it a valuable tool for oncology, apoptosis, and cell cycle research. Beyond this product, CamelBio can supply validated antibody pairs, optimized monoclonal and polyclonal antibodies, bulk ancillary reagents, and rare‑target raw‑material sourcing to support your entire assay development pipeline—from concept to clinic.