P53 and cancer

Abstract

p53 acts as the single most important gene in cancer as a single mutation can lead to tumorigenesis. More recently p53 functions have been further diversified by the discovery of various isoforms of p53. These isoforms derived either by alternative splicing or by differential translational sites are expressed in a tissue specific manner and have been proposed to influence p53 activity. Here we are trying to confirm the influence of p53β isoform on p53 activity either by its transcriptional repression or by forming a complex with p53 thereby modulating its activity at p53 dependent promoters. Expression of both p53 and its isoform rules out the chances of transcriptional regulation. Therefore, it may be that p53β/p53 may be binding differentially to p53 dependent promoters producing aberrations.