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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 ]
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.
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.
The apoptin protein, also known as viral protein 3 (VP3), was first isolated from chickens and has been found to cause programmed cell death in human cancer cells. [ citation needed ] Apoptin induces apoptosis, or cell death, in deformed or cancerous cells independently of a protein called p53 , meaning it is active in cells deficient of p53 ...
The p53 upregulated modulator of apoptosis (PUMA) also known as Bcl-2-binding component 3 (BBC3), is a pro-apoptotic protein, member of the Bcl-2 protein family. [5] [6] In humans, the Bcl-2-binding component 3 protein is encoded by the BBC3 gene. [5] [6] The expression of PUMA is regulated by the tumor suppressor p53.
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 ]
Tumors cells often have inactivated the machinery that is required for apoptosis such as the p53 protein. [4] This is usually achieved by mutations in the p53 protein or by loss of the chromosome region that contains the genetic code for it. [21] p53 acts to prevent the propagation of tumor cells and is considered a major tumor suppressor protein.
In adaptation to higher tendency of cell death, blind mole rats evolved a mutation in the tumor suppressor protein p53 (which is also used in humans) to prevent cells from undergoing apoptosis. Human cancer patients have similar mutations, and blind mole rats were thought to be more susceptible to cancer because their cells cannot undergo ...