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PUMA has been shown to be active in inducing apoptosis in hematopoietic and intestinal tissue following γ-irradiation. [12] [55] Since inhibition of PUMA does not directly cause spontaneous malignancies, therapeutics to inhibit PUMA function in healthy tissue could lessen or eliminate the side effects of traditional cancer therapies. [7]
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 ]
Neurodegenerative diseases such as Alzheimer's, Parkinson's, and Huntington's are all age-related diseases and involve increased apoptosis where cells die that are still able to function or that contribute to support function of tissue. Apaf-1-ALT is an Apaf-1 mutant found in prostate cancer, which does not have residues 339-1248.
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. [88] 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 ...
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.
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 .
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]
P53, p63, and p73 have similar features in their gene structures and functions but have also diverged evolutionarily. The p53 family evolved from an ancestor gene in unicellular life. [ 4 ] The ancestor gene functioned in germ line DNA protection early invertebrates. [ 5 ]