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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 ]
It is the physiological inhibitor of MDM2, an E3 ubiquitin ligase controlling the activity and stability of P53, and loss of P14ARF activity may have a similar effect as loss of P53. [16] P14ARF induces cell cycle arrest in G2 phase and subsequent apoptosis in a P53-dependent and P53-independent manner, and thus is regarded as a tumor suppressor.
The p53 p63 p73 family is a family of tumor suppressor genes. [1] [2] This gene family codes the proteins: p53; TP73L (also known as "p63") p73; They are sometimes considered part of a "p53 family." When overexpressed, these proteins are known to be involved in tumor pathogenesis. [3]
The exact targets for LOH are not characterised for all chromosomal losses in cancer, but certain are very well mapped. Some examples are 17p13 loss in multiple cancer types where a copy of TP53 gene gets inactivated, 13q14 loss in retinoblastoma with RB1 gene deletion or 11p13 in Wilms' tumor where WT1 gene is lost. [2]
H1299, also known as NCI-H1299 [1] [2] or CRL-5803, [3] is a human non-small cell lung carcinoma cell line derived from the lymph node, which is widely used in research. [4]As with other immortalized cell lines, H1299 cells can divide indefinitely.
The mutation of the P53 gene is the most common gene mutation found in cancer cells. A study has shown that p53 mutations are common in tobacco-related cancers, with a variation in the amount of G-T transversions in lung cancer from smokers and non-smokers.
PMS2 is a protective mediator of cell survival in p53-deficient cells and modulates protective DNA damage response pathways independently of p53. [16] PMS2 and MLH1 can protect cells from cell death by counteracting p73-mediated apoptosis in a mismatch repair dependent manner.
Once stabilized, p53 can exert its tumor suppression function. Downstream pathways of p53 act to either halt cell cycle progression in G1 or G2 phases of the cell cycle [48] or promote cell-death, depending on the severity of the DNA damage. [49] See schematic of the role of USP7 in the p53-dependent pathway.
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