Mutation is required to activate the p53 gene for cooperation with the ras oncogene and transformation.

摘要: Previous experiments have brought into question which amino acid sequence of the p53 oncogene product should be considered wild type and whether normal protein is capable cooperating with ras to transform cells in culture. To address these questions, a series cDNA-genomic hybrid clones been compared for ability cooperate transformation assays. From experiments, it has become clear that alanine at position 135, either genomic clone or cDNA clone, failed produce cooperated transformed cells. Replacing valine this activated assay. Using restriction enzyme polymorphisms gene, was shown mouse DNA encodes 135 protein. Thus, mutation required activate cooperation oncogene. After cotransfection always produced more cell foci (1.7-fold) than similar were readily cloned (3.6-fold) permanent lines. A deletion mutants employed show presence intron 4 gene sufficient provide much enhanced clonability from culture dishes. The introns constructions also resulted elevated levels p53-plus-ras-transformed qualitative changes are ras. Quantitative improvements frequencies associated higher expression altered provided by having one transforming plasmid.