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p53, also known as Tumor protein P53, cellular tumor antigen p53 (UniProt name), or transformation-related protein 53 (TRP53) is a regulatory protein that is often mutated in human cancers. The p53 proteins (originally thought to be, and often spoken of as, a single protein) are crucial in vertebrates , where they prevent cancer formation. [ 5 ]
Activation of a suicide gene can cause death through a variety of pathways, but one important cellular "switch" to induce apoptosis is the p53 protein. Stimulation or introduction (through gene therapy ) of suicide genes is a potential way of treating cancer or other proliferative diseases.
Even though PUMA function is compromised in most cancer cells, it does not appear that genetic inactivation of PUMA is a direct target of cancer. [ 36 ] [ 37 ] [ 38 ] Many cancers do exhibit p53 gene mutations, making gene therapies that target this gene [ clarification needed ] impossible, but an alternate pathway may be to focus on ...
Deficient expression of DNA repair proteins due to an inherited mutation can cause increased risk of cancer. Individuals with an inherited impairment in any of 34 DNA repair genes (see article DNA repair-deficiency disorder) have an increased risk of cancer, with some defects causing up to a 100% lifetime chance of cancer (e.g. p53 mutations ...
P53, p63, and p73 have similar features in their gene structures and functions but have also diverged evolutionarily. The p53 family evolved from an ancestor gene in unicellular life. [ 4 ] The ancestor gene functioned in germ line DNA protection early invertebrates. [ 5 ]
This stabilizes p53 and causes a large increase in p53 concentration. Additionally, p53 bound to E1B-55k has an affinity for its binding site that is ten times higher than free p53. [ 8 ] Presumably, this increased affinity and concentration of p53 turns the p53-E1B-55k complex into a powerful repressor.
Tumor suppressor p53-binding protein 1 also known as p53-binding protein 1 or 53BP1 is a protein that in humans is encoded by the TP53BP1 gene. [ 5 ] [ 6 ] [ 7 ] Clinical significance
HT-29 cells overproduce the p53 tumor antigen, but have a mutation in the p53 gene at position 273, resulting in a histidine replacing an arginine. The cells proliferate rapidly in media containing suramin , with corresponding high expression of the c-myc oncogene.