Tumor suppressor p53 has the capability to induce cell cycle arrest and has a role in DNA repair, senescence and apoptosis. It binds to Simian vacuolating virus 40 (SV40) T-antigen and human papilloma virus E6 protein. The p53 gene is mutated in various cancers, such as of the breast, ovarian, bladder, colon and lung.', 'p53 was identified as a tumor suppressor by showing th at this protein has the ability to block transformation and to inhibit tumor cell growth. In addition, p53 is a transcription factor capable of regulating the expression of a subset of downstream genes. Mutation of two specific N-terminal residues in p53 (residues Leu22 and Trp23) impairs the ability of p53 to transactivate and has been correlated with its ability to bind TAFII40 and TAFII60 (or TAFII31 and TAFII70) suggesting th at one or both of these interactions is important for activation. Mutation of residues 22 and 23 to Ala does not affect binding to TBP, although mutation of these residues to charged amino acids has been reported to disrupt the p53-TBP interaction. Different mutations in p53 gene have been characterized in a variety of human cancers. Loss or mutation of p53 function is highly correlated with tumorigenesis.
