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The antioxidant function of the p53 tumor suppressor
TLDR
It is shown that p53 protects the genome from oxidation by reactive oxygen species (ROS), a major cause of DNA damage and genetic instability, and relatively low levels of p53 are sufficient for upregulation of several genes with antioxidant products, which is associated with a decrease in intracellular ROS.
Restoration of the tumor suppressor function to mutant p53 by a low-molecular-weight compound
TLDR
This work found one compound capable of inducing apoptosis in human tumor cells through restoration of the transcriptional transactivation function to mutant p53, named PRIMA-1, which rescued both DNA contact and structural p53 mutants in vitro and in living cells.
Regeneration of Peroxiredoxins by p53-Regulated Sestrins, Homologs of Bacterial AhpD
TLDR
It is shown that sestrins, a family of proteins whose expression is modulated by p53, are required for regeneration of Prxs containing Cys-SO2H, thus reestablishing the antioxidant firewall.
The candidate tumour suppressor p33ING1cooperates with p53 in cell growth control
TLDR
The results indicate that p33ING1 is a component of the p53 signalling pathway that cooperates with p53 in the negative regulation of cell proliferation by modulating p53-dependent transcriptional activation.
Use of genetic suppressor elements to dissect distinct biological effects of separate p53 domains.
TLDR
It is suggested that processes related to control of senescence, response to DNA damage, and transformation involve different functions of the p53 protein and furthermore indicate a regulatory role for the 3'-untranslated region of p53 mRNA.
Small-molecule RETRA suppresses mutant p53-bearing cancer cells through a p73-dependent salvage pathway
TLDR
A small-molecule RETRA is described that activates a set of p53-regulated genes and specifically suppresses mutant p 53-bearing tumor cells in vitro and in mouse xenografts and validate the mutant p53–p73 complex as a promising and highly specific potential target for cancer therapy.
Repression of sestrin family genes contributes to oncogenic Ras-induced reactive oxygen species up-regulation and genetic instability.
TLDR
Changes in expression of sestrins can represent an important determinant of genetic instability in neoplastic cells showing simultaneous dysfunctions of Ras and p53, and several Ras effectors independently mediate ROS up-regulation.
p53 Pathway in Renal Cell Carcinoma Is Repressed by a Dominant Mechanism
TLDR
Consistently, p53 inactivation prevailed in the hybrids of RCC cells with the cells possessing fully functional p53, and cells of normal kidney epithelium also caused partial p53 repression in cell fusion experiments, suggesting that RCC-specific p 53 repression may be based on an unknown dominant mechanism also acting in normal kidney tissue.
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