The antioxidant function of the p53 tumor suppressor

By A. Sablina, A. Budanov, G. Ilyinskaya, L. Agapova, J. Kravchenko, P. Chumakov. Nature Medicine, 2005

1,113 citations recorded by the source corpus.

Subfields: Biotechnology, Cancer Research, Oncology

View Paper: https://www.semanticscholar.org/paper/53b95ba72cc497dcb6c23c6773e02b7d3bcfd01c

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Citations in the corpus

Regulation of reactive oxygen species generation in cell signaling (2011, background): “Interestingly, p53 plays a role in the maintenance of redox homeostasis by controlling the expression of antioxidant genes, such as SESN1 (mammalian sestrin homologue), SESN2, glutathione peroxidase-1 (GPX1), and TP53INP1 (Cano et al., 2009; Sablina et al., 2005; Stambolsky et al., 2006; Tomko et al”
Blinded by the Light: The Growing Complexity of p53. (2009, background): “antioxidants by decreasing the levels of intracellular reactive oxygen species (Liu et al., 2008; Sablina et al., 2005).”
Oxidative stress: an essential factor in the pathogenesis of gastrointestinal mucosal diseases. (2014, background): “GPX1 is ubiquitous, but GPX2 has epithelium-specific expression.”
ROS and p53: a versatile partnership. (2008, background): “Suppression of p53 results in a significant decrease in the basal transcriptions of SESN1, SESN2, and GPX1 without affecting the expression of pro-oxidant genes BAX, NQO1, and PUMA [27].”
Macrophage Dysfunction Impairs Resolution of Inflammation in the Wounds of Diabetic Mice (2010, methodology): “The first group was supplemented (intragastric, daily once) with Nacetylcysteine (NAC) at a dose of 1 mg/g body weight [19,20].”
ROS as signalling molecules: mechanisms that generate specificity in ROS homeostasis (2007, background): “…component of the p53 tumour-suppressor function relies on a newly discovered antioxidant function. p53 prevents the accumulation of damage that could be caused by the continuous endogenous production of H 2 O 2 by regulating GPX1 and ses-trins, which are sulphiredoxin functional homologues 81 .”
Myeloid-derived Suppressor Cells Inhibit T Cell Activation by Depleting Cystine and Cysteine (2009, background): “In vivo experiments using mice with progressively growing tumors have shown therapeutic efficacy (42, 43).”
Enrichment of tomato fruit with health-promoting anthocyanins by expression of select transcription factors (2008, background): “Trp53 −/− knockout mice have an average life expectancy of about 140 d, although long-term dietary administration of strong antioxidants such as N-acetylcysteine (NAC) can significantly reduce the incidence of tumor induction and prolong their lifespa”
Phosphate-activated glutaminase (GLS2), a p53-inducible regulator of glutamine metabolism and reactive oxygen species (2010, background): “p53 has been reported to have opposing roles in the regulation of ROS through transactivation of antioxidant and prooxidant genes, each of which contribute to the tumor suppressor function of p53 (19, 20).”
Akt determines replicative senescence and oxidative or oncogenic premature senescence and sensitizes cells to oxidative apoptosis (2008, background): “Sesn1 and Sesn2 are p53 target genes and are responsible for the resistance to oxidative stress induced by p53 both in vitro and in vivo (Budanov et al., 2002; Matheu et al., 2007; Sablina et al., 2005).”
Trends in oxidative aging theories. (2007, background): “It was recently discovered that p53 regulates the expression of multiple antioxidant genes and that p53 mice have elevated oxidative stress [329].”
Targeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach? (2009, background): “Furthermore, p53 also acts as a transcription factor to regulate the expression of many pro-oxidant and antioxidant gene”
ROS Generation and Antioxidant Defense Systems in Normal and Malignant Cells (2019, background): “Moreover, the authors have demonstrated that p53 induction is associated with the excessive ROS release by mitochondria, which supports its prooxidant role [235].”
TIGAR, a p53-inducible regulator of glycolysis and apoptosis. (2006, background): “…to regulate TIGAR expression. p53-inducible genes can be broadly placed into two groups: those induced rapidly by low levels of stress (generally cell-cycle arrest or antioxidant targets) and those that are induced by higher levels of p53/stress (generally apoptotic targets) (Sablina et al., 2005).”
A low level of reactive oxygen species selects for primitive hematopoietic stem cells that may reside in the low-oxygenic niche. (2007, background): “In the ROS population enriched for long-term self renewing cells, the role of p21 seems to maintain the quiescence(36) and the low level of p53 may have more to do with antioxidant function and decreasing the intracellular ROS level.(34) Since hematopoietic exhaustion has been reported to be acceler”
Cellular senescence in cancer and aging. (2007, positive): “Finally, in agreement with the antioxidant function of p53 (Sablina et al., 2005), increased activity of p53 by combination of extra gene dosage of p53 and ARF decreases the amount of oxidative damage in aged mice and delays aging (Matheu et al., 2007).”
Glutaminase 2, a novel p53 target gene regulating energy metabolism and antioxidant function (2010, background): “The antioxidant role of p53 is important to reduce oxidative stress-induced DNA damage and mutations, which contributes greatly to the tumor suppression activity of p53 (5).”
Reactive Oxygen Species in Health and Disease (2012, background): “The lost response was restored by introducing normal mitochondria into the rho0 β-cells, confirming the mitochondrial origin of the defect [73].”