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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 ]
Though smoking leads to an overall decrease in DNA methylation, several critical genes become hypermethylated. Two of the most noteworthy of these genes are p16 and p53 . These genes are critical to cell cycle regulation and were shown to have higher levels of methylation in smokers than in non smokers. [ 3 ]
The mutation of the P53 gene is the most common gene mutation found in cancer cells. A study has shown that p53 mutations are common in tobacco-related cancers, with a variation in the amount of G-T transversions in lung cancer from smokers and non-smokers.
Passive smoking is the ... linked the occurrence of feline oral cancer to exposure to environmental tobacco smoke through an overexpression of the p53 gene. ...
This gene is a transcription factor that regulates the cell cycle and hence functions as a tumor suppressor. The anti-benzo[a]pyrene diol epoxides induce guanine to thymine transversions in related areas of p53, thereby inactivating its tumor suppression ability in certain cells, leading to genetic mutations and potentially to cancer. [6]
The p53 p63 p73 family is a family of tumor suppressor genes. [1] [2] This gene family codes the proteins: p53; TP73L (also known as "p63") p73; They are sometimes considered part of a "p53 family." When overexpressed, these proteins are known to be involved in tumor pathogenesis. [3]
When there is too much damage, apoptosis is triggered in order to protect the organism from potentially harmful cells.7 p53, also known as a tumor suppressor gene, is a major regulatory protein in the DNA damage response system which binds directly to the promoters of its target genes. p53 acts primarily at the G1 checkpoint (controlling the G1 ...
The Warburg effect is the preferential use of glycolysis for energy to sustain cancer growth. p53 has been shown to regulate the shift from the respiratory to the glycolytic pathway. [102] However, a mutation can damage the tumor suppressor gene itself, or the signal pathway that activates it, "switching it off".