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Mouse Monoclonal to p53 (Phospho-Ser392)

FP3.2 [FPS392] (IgG1)

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The tumour suppressor protein p53 is a key element of intracellular anticancer protection. It mediates cell cycle arrest or apoptosis in response to DNA damage or to starvation for pyrimidine nukleotides. It is up-regulated in response to these stress signals and stimulated to activate transcription of specific genes, resulting in expression of p21waf1 and other proteins involved in G1 or G2/M arrest, or proteins that trigger apoptosis, such as Bcl-2. The structure of p53 comprises N-terminal transactivation domain, central DNA-binding domain, oligomerisation domain, and C-terminal regulatory domain. There are various phosphorylation sites on p53, of which the phosphorylation at Ser15 is important for p53 activation and stabilization.


The antibody FP3.2 [FPS392] reacts with human p53 tumour suppressor protein phosphorylated at CKII site (Ser 392).

Regulatory Status


KLH-conjugated phosphopeptide RHKKLMFKTEGPDS[P]D, corresponding to amino acids 378-393 of human p53.

Species Reactivity:

  • Human

Negative Species:


  • Western Blotting
    Recommended dilution: 1 μg/ml
  • Immunohistochemistry (paraffin sections)
    Staining technique: standard ABC technique (DAB+)
    Pretreatment: high temperature antigen retrieval (microwave, pressure cooker) in 10 mM citrate buffer pH 6.0 or 1 mM EDTA-NaOH buffer pH 8.0
    Recommended dilution: 10 μg/ml
    Incubation:1 hour at RT; or overnight at 4░C
    Positive tissue: breast carcinoma with high level of wild-type p53
Usage note:
Indicated dilutions are recommended starting points for use of this product. Working concentrations should be determined by the investigator.

General references

  • *Agarwal ML, Agarwal A, Taylor WR, Stark GR: p53 controls both the G2/M and the G1 cell cycle checkpoints and mediates reversible growth arrest in human fibroblasts. Proc Natl Acad Sci U S A. 1995 Aug 29;92(18):8493-7. [Abstract] [Full Text]
  • *Agarwal ML, Agarwal A, Taylor WR, Chernova O, Sharma Y, Stark GR: A p53-dependent S-phase checkpoint helps to protect cells from DNA damage in response to starvation for pyrimidine nucleotides. Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14775-80. [Abstract] [Full Text]
  • *Taylor WR, DePrimo SE, Agarwal A, Agarwal ML, Sch÷nthal AH, Katula KS, Stark GR: Mechanisms of G2 arrest in response to overexpression of p53. Mol Biol Cell. 1999 Nov;10(11):3607-22. [Abstract] [Full Text]
  • *Taylor WR, Agarwal ML, Agarwal A, Stacey DW, Stark GR: p53 inhibits entry into mitosis when DNA synthesis is blocked. Oncogene. 1999 Jan 14;18(2):283-95. [Abstract] [Full Text]
  • *Tanigawa S, Fujii M, Hou DX: Stabilization of p53 is involved in quercetin-induced cell cycle arrest and apoptosis in HepG2 cells. Biosci Biotechnol Biochem. 2008 Mar;72(3):797-804. [Abstract] [Full Text]
  • Product Specific References

  • *Blaydes JP, Craig AL, Wallace M, Ball HM, Traynor NJ, Gibbs NK, Hupp TR: Synergistic activation of p53-dependent transcription by two cooperating damage recognition pathways. Oncogene. 2000 Aug 10;19(34):3829-39. [Abstract]
  • For research use only. Not for drug, diagnostic or other use.

    Related Products

  • Mouse IgG1 Isotype Control
  • Example Data

    Fig. 1A
    Fig. 1B

    Fig. 1. Immunohistochemistry staining of Wild-type p53 expressed in human trophoblast (paraffin-embedded sections).
    1A – anti-p53 (total)
    1B – anti-p53 (phospho Ser392)
    Note that some of total p53 positive nuclei are also FP3.2 (phospho p53) positive.

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