Essential role for the peroxiredoxin Prdx1 in erythrocyte antioxidant defence and tumour suppression

By C. Neumann, D. Krause, C. Carman, Shampa Das, D. Dubey, J. L. Abraham, R. Bronson, Y. Fujiwara, Stuart H. Orkin, R. A. Etten. Nature, 2003

810 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/51264cd7d382e0eec2e737b5068ec3987e6ace0a

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Citations in the corpus

Oxidative Stress in Cancer (2020, background): “Specifically, Prdx1−/− and Prdx1+/− mice exhibit increased oxidative DNA damage, and the aging mutant mice exhibit a higher spontaneous incidence of hepatocellular carcinoma, fibrosarcoma, osteosarcoma, islet cell adenoma, lung adenocarcinoma, and breast adenocarcinoma than age-matched Prdx1+/+ mice”
Mitochondrial Energetics and Therapeutics (2010, positive): “Also Prx1 null myocyte-enhancing factors proliferate slowly and are more sensitive to oxidative stress (161).”
The Roles of NRF2 in Modulating Cellular Iron Homeostasis (2017, background): “Importantly, players in these systems such as the peroxiredoxins have been shown to be particularly efficient ROS scavengers (9, 55) capable of affecting both physiological iron homeostasis and erythrocyte health (95, 109).”
The autophagy protein Atg7 is essential for hematopoietic stem cell maintenance (2011, background): “Not surprisingly, mice lacking the antioxidant enzyme Prdx1 have a shortened lifespan, suffer from hemolytic anemia, and develop hematological malignancies (Neumann et al., 2003).”
Mitochondrial reactive oxygen species and cancer (2014, background): “Interestingly, while NRF2 loss inhibited tumor formation, mice deficient for the antioxidant PRX1 have increased ROS and display decreased life span due to hemolytic anemia and development of malignant cancers [33].”
Cadmium stress: an oxidative challenge (2010, positive): “They are found in bacteria, plants and mammals and are shown to be important in normal ageing as mice lacking Prx 1 or 2 are viable and fertile, but have shortened life span owing to the development of severe hemolytic anemia and several malignant cancers (Neumann et al. 2003).”
Is the Oxidative Stress Theory of Aging Dead? (2009, background): “For example, peroxiredoxin-1 (Prdx1) knockout mice (B6), are shown to have a significantly shortened lifespan; however, this effect is due mainly to a higher incidence in cancer burden (osteosarcoma, fibrosarcoma) and hemolytic anemia, which are not pathologies found in this strain of mice [86].”
Trends in oxidative aging theories. (2007, background): “Interestingly, the Prxd1 heterozygous knockout mice show an increased tumor burden but no decrease in life span compared to wild-type mice [229], a result similar to the life span and pathology study in Sod2 mice [212].”
Reactive oxygen species in tumor progression. (2005, neutral): “development of several malignant cancers (84).”
Signal transduction by reactive oxygen species (2011, background): “Consistent with these latter observations, Prx1 appears to act as a bone fide tumor suppressor as whole body or conditional Prdx1 knockout mice exhibit altered PTEN activity (Cao et al., 2009) with a resulting increased rate of tumor formation (Neumann et al., 2003; Cao et al., 2009).”
Inactivation of peroxiredoxin I by phosphorylation allows localized H(2)O(2) accumulation for cell signaling. (2010, positive): “Functional differences between PrxI and PrxII are also apparent in the phenotypes of the corresponding knockout mice: mice lacking PrxI thus manifest an increased susceptibility to cancer, whereas those deficient in PrxII do not (Neumann et al., 2003).”
Reactive oxygen species in cancer (2010, background): “Interestingly, PrxI knockout mice show increased levels of oxidative stress and die prematurely of cancer [43].”
ROS Function in Redox Signaling and Oxidative Stress (2014, background): “Since this PRX1 inactivation is localized to membranes it allows intracellular PRX1 pools to remain active, thus preventing peroxide build up in the cells.”