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p53Tumor Suppressor Gene
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The researchers compared cells cultured from mice that did not express the p53 gene with cells that came from normal mice.
The rare p53 polymorphism analyzed in this study is found almost exclusively in populations of African descent.
Therefore, the study was performed to assess the immunohistochemical expression of p53 in oral tumorogenesis and to assess the degree of p53 expression form of dysplasia to malignancy.
1,2 Although the functional role of S100B in carcinogenesis is still not fully understood, several studies have demonstrated that the elevated levels of this protein play a role in cell proliferation by down regulating P53 protein.
The report provides a snapshot of the global therapeutic landscape for Cellular Tumor Antigen P53 (Tumor Suppressor P53 or Antigen NY-CO-13)
Immunohistochemical staining performed on 4-[micro]m, formalin-fixed, paraffin-embedded sections using P53 & Caspase 3 antibodies at 1:50 dilution (DAKO, Carpinteria, CA).
In addition, resveratrol has been shown to deacetylate p53 by activating the SIRT1 pathway, reducing cisplatin-induced injury to proximal tubular epithelial cells in mice [9], and doxorubicin-induced myocardial apoptosis [10].
53BP1 is a mediator of Chk2 and p53 activation, and its recruitment depends on phosphorylation of H2AX.
The P53 pathway seems to play a critical role in therapeutic response both as a diagnostic and marker in the prognosis of therapeutic treatment effects.
Breast cancer genome analyses have shown that there are a few tumour suppressor genes that are frequently mutated such as breast cancer 1, early onset (BRCA1) and tumour protein p53 (TP53) genes (2).
The parameters used to analyze the expression of both p53 and ki67 antigen are:
The p53 protein is composed of 393 residues and is divisible into three structural domains.