This mAb reacts with an N-terminal epitope (aa 32-79) of both wild type and mutated p53. Mutation and/or allelic loss of p53 is one of the causes of a variety of mesenchymal and epithelial tumors. If it occurs in the germ line, such tumors run in families. In most transformed and tumor cells the concentration of p53 is increased 5-1000 fold over the minute concentrations (1000 molecules cell) in normal cells, principally due to the increased half-life (4 h) compared to that of the wild-type (20 min). It localizes in the nucleus, but is detectable at the plasma membrane during mitosis and when certain mutations modulate cytoplasmic/nuclear distribution. Mutations arise with an average frequency of 70% but incidence varies from zero in carcinoid lung tumors to 97% in primary melanomas. High concentrations of p53 protein are transiently expressed in human epidermis and superficial dermal fibroblasts following mild ultraviolet irradiation. Positive nuclear staining with specific antibody has been reported to be a negative prognostic factor in breast carcinoma, lung carcinoma, colorectal, and urothelial carcinoma. Anti-p53 positivity has also been used to differentiate uterine serous carcinoma from endometrioid carcinoma as well as to detect intratubular germ cell neoplasia.

Variations in protocols, secondaries and substrates may require the p53 antibody to be titered up or down for optimal performance.

1.The prediluted format is supplied in a dropper bottle and is optimized for use in IHC. After epitope retrieval step (if required), drip mAb solution onto the tissue section and incubate at RT for 30 min.

Human p53 beta-galactosidase fusion protein was used as the immunogen for this antibody. Its epitope maps near the N-terminal end (aa 32-79) of p53.

Store the p53 antibody at 2-8oC (with azide) or aliquot and store at -20oC or colder (without azide).