Forkhead transcription factor FOXO3a protects quiescent cells from oxidative stress

By G. Kops, T. Dansen, Paulien E. Polderman, I. Saarloos, K. Wirtz, P. Coffer, Ting-Ting Huang, J. Bos, R. Medema, B. Burgering. Nature, 2002

1,629 citations recorded by the source corpus.

Subfields: Aging, Molecular Biology, Plant Science

View Paper: https://www.semanticscholar.org/paper/ebc30bab787a3844fb97a794c415b95eaf6c309b

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In Aging

1. D. Sinclair
2. A. Brunet
3. V. Longo
4. L. Guarente
5. C. Kenyon
6. G. Lithgow
7. Rute Martins
8. W. Link

In Molecular Biology

1. W. Gu
2. J. Villén
3. Steven P. Gygi
4. L. Guarente
5. A. Brunet
6. D. Sinclair
7. N. Hay
8. C. Kenyon

In Plant Science

1. Mark P. Mattson
2. V. Longo

Citations in the corpus

• Redox regulation of FoxO transcription factors (2015, background): “In humans, these FoxO-regulated antioxidants include Mn-SOD (SOD-2) [11], catalyzing disproportionation (dismutation) of the first oxygen reduction product, superoxide, to generate oxygen and hydrogen peroxide (H2O2).”
• The plasticity of aging: insights from long-lived mutants. (2005, background): “Likewise, mammalian FOXO proteins activate stress-response genes when insulin or IGF-1 levels are reduced (Kops et al., 2002; Nemoto and Finkel, 2002; Tran et al., 2002).”
• Sirt3 blocks the cardiac hypertrophic response by augmenting Foxo3a-dependent antioxidant defense mechanisms in mice. (2009, background): “The expression levels of both MnSOD and catalase have been shown to be controlled by the Foxo group of transcription factors (39, 40).”
• FoxOs are critical mediators of hematopoietic stem cell resistance to physiologic oxidative stress. (2007, background): “In addition, the oxidative stress response is regulated in part by FoxO induction of MnSOD, catalase, and GADD45 (Kops et al., 2002a; Nemoto and Finkel, 2002; Tran et al., 2002), and has been linked to longevity and dauer formation in C. elegans (Honda and Honda, 1999; Lee et al., 2003; Murphy et al”
• FoxO transcription factors in the maintenance of cellular homeostasis during aging. (2008, background): “FoxO-dependent transcription plays an important role in a wide variety of cellular outputs, including glucose metabolism, cell cycle arrest, differentiation, detoxification of reactive oxygen species (ROS), repair of damaged DNA, and apoptosis [17–26].”
• Akt determines replicative senescence and oxidative or oncogenic premature senescence and sensitizes cells to oxidative apoptosis (2008, background): “Consistently, levels of both manganese superoxide dismutase (MnSOD) and catalase, two known targets of FoxO (Kops et al., 2002; Nemoto and Finkel, 2002), were elevated in Akt1/2 DKO MEFs (Figure 3A).”
• A conserved MST-FOXO signaling pathway mediates oxidative-stress responses and extends life span. (2006, positive): “The FOXO transcription factors induce apoptotic or adaptive responses in mammalian cells upon exposure to oxidative stress (Brunet et al., 2004; Kops et al., 2002).”
• Neuroprotective role of SIRT1 in mammalian models of Huntington’s disease through activation of multiple SIRT1 targets (2011, positive): “Foxo3a is highly expressed in adult brain, and recent work indicates that Foxo3a has key roles in neuronal survival under both basal and disease conditions 33–35 .”
• Peroxisomes and oxidative stress. (2006, background): “More recently, the involvement of MnSOD in plant senescence was reported, and it was found that the mitochondrial and peroxisomal enzyme are differentially regulated [69].”