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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]
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 ]
P53 causes cells to enter apoptosis and disrupt further cell division therefore preventing that cell from becoming cancerous (16). In the majority of cancers it is the p53 pathway that has become mutated resulting in lack of ability to terminate dysfunctional cells.
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 ...
Apoptosis (from Ancient Greek: ἀπόπτωσις, romanized: apóptōsis, lit. 'falling off') is a form of programmed cell death that occurs in multicellular organisms and in some eukaryotic, single-celled microorganisms such as yeast. [1] Biochemical events lead to characteristic cell changes and death. [2]
[21] p53 works by either halting progression through the cell cycle when uncontrolled cell division is sensed or it can promote cell death through apoptosis in the presence of irreparable DNA damage. [21] Mitotic catastrophe can occur in a p53 independent fashion and thus presents a therapeutic avenue of interest. [4]
P53, a transcription factor, can bind two sites within the human TIGAR gene to activate expression. [9] [13] One site is found within the first intron, and binds p53 with high affinity. [9] [13] The second is found just prior to the first exon, binds p53 with low affinity, [9] [13] and is conserved between mice and humans. [9]
The expression of BID is upregulated by the tumor suppressor p53, and BID has been shown to be involved in p53-mediated apoptosis. [7] The p53 protein is a transcription factor that, when activated as part of the cell's response to stress, regulates many downstream target genes, including BID. However, p53 also has a transcription-independent ...