Anti-p53 / TP53 (N-Terminal Region), clone PAb 1801

0.2 mg/ml in 1X PBS with 0.1 mg/ml BSA (US sourced) and 0.05% sodium azide. 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. Protein function: Acts as a tumor suppressor in many tumor types, induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. In cooperation with mitochondrial PPIF is involved in activating oxidative stress-induced necrosis, the function is largely independent of transcription. Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA- Mkln1. LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis and seem to have to effect on cell-cycle regulation. Implicated in Notch signaling cross-over. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Isoform 2 enhances the transactivation activity of isoform 1 from some but not all TP53-inducible promoters. Isoform 4 suppresses transactivation activity and impairs growth suppression mediated by isoform 1. Isoform 7 inhibits isoform 1-mediated apoptosis. Regulates the circadian clock by repressing CLOCK-ARNTL/BMAL1- mediated transcriptional activation of PER2 (PubMed:24051492). [The UniProt Consortium]