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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.
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 .
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.
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 ]
As survivin is a known inhibitor of apoptosis, it can be implied that p53 repression of survivin is one mechanism by which cells can undergo apoptosis upon induction by apoptotic stimuli or signals. When survivin is over-expressed in the cell lines mentioned in the previous paragraph, apoptotic response from DNA-damaging agent adriamycin ...
Cape Cod Healthcare has seen a 15% increase in the number of patients who receive all their cancer treatment at its facilities, CEO Mike Lauf says. 'One-stop shopping.' Cancer care on Cape Cod to ...
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]