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This increase in PUMA levels induces apoptosis through mitochondrial dysfunction. p53, and with it PUMA, is activated due to DNA damage caused by a variety of genotoxic agents. Other agents that induce p53 dependent apoptosis are neurotoxins, [16] [17] proteasome inhibitors, [18] microtubule poisons, [19] and transcription inhibitors. [20]
While apoptosis is required for natural body function, mutations of the apoptosome pathway cause catastrophic effects and changes in the body. Mutations of the cell pathway can either promote cell death or disallow cell death creating a huge amount of disease in the body.
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 ]
Part of this pathway includes alpha-interferon and beta-interferon, which induce transcription of the p53 gene, resulting in the increase of p53 protein level and enhancement of cancer cell-apoptosis. [85] p53 prevents the cell from replicating by stopping the cell cycle at G1, or interphase, to give the cell time to repair; however, it will ...
In the field of genetics, a suicide gene is a gene that will cause a cell to kill itself through the process of apoptosis (programmed cell death). 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.
High-normal levels of the bile acid deoxycholic acid cause apoptosis in human colon cells, [56] but may also lead to colon cancer if repair and apoptotic defenses are insufficient. [57] Apoptosis serves as a safeguard mechanism against tumorigenesis. [58] It prevents the increased mutagenesis that excess DNA damage could cause, upon replication ...
Overview of signal transduction pathways involved in apoptosis. Cell death is the event of a biological cell ceasing to carry out its functions. This may be the result of the natural process of old cells dying and being replaced by new ones, as in programmed cell death, or may result from factors such as diseases, localized injury, or the death of the organism of which the cells are part.
E1B-55k blocks p53 from inhibiting cell cycling and stops it from inducing apoptosis. [7] Observations show that E1b-55k inhibits activation by p53 by binding a repression domain to it, converting it from an activator to a repressor of p53-activated genes. This stabilizes p53 and causes a large increase in p53 concentration.