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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 ]
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.
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.
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 ...
It induces apoptosis through a pathway that involves mitochondria but does not rely on the p53 protein or death receptors typically involved in cell death. [7] In healthy cells, apoptin stays in the cytoplasm, but in cancer cells, it moves to the nucleus after being activated by a process called phosphorylation.
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 ...
Normally, TIGAR manufactured by the body is activated by the p53 tumour suppressor protein after a cell has experienced a low level of DNA damage or stress. In some cancers, TIGAR has fallen under the control of other proteins. The hope is that future research into TIGAR will provide insight into new ways to treat cancer. [8] [9] [10]
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 ...