Anti-p53 Monoclonal Antibody (Clone:BP53-12)

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. 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 seems to have an 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]