The FoxO code
By Daniel R. Calnan, A. Brunet. Oncogene, 2008
1,204 citations recorded by the source corpus.
Subfields: Aging, Geriatrics and Gerontology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/1b65d92b99d1f6284a41fb948c64c9a400af3430
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In Aging
In Geriatrics and Gerontology
In Molecular Biology
Citations in the corpus
- Cellular and molecular mechanisms of muscle atrophy (2013, background): “As predicted, the reduced activity of the Akt pathway observed in different models of muscle atrophy results in decreased levels of phosphorylated FoxO in the cytoplasm and a marked increase of nuclear FoxO (reviewed in Calnan and Brunet, 2008) (Fig.”
- FoxO transcription factors; Regulation by AKT and 14-3-3 proteins. (2011, background): “There are 4 mammalian FoxO members designated FoxO1/FKHR/ FoxO1a, FoxO3/FKHRL1/FoxO3a, FoxO4/AFX and FoxO6, sharing high protein homology (reviewed in [1,2]; for the Fox gene nomenclature”
- Long live FOXO: unraveling the role of FOXO proteins in aging and longevity (2015, background): “…mainly as transcriptional activators by binding the consensus core recognition motif TTGTTTAC, and their activity is inhibited by the IIS pathway (Biggs et al., 1999; Brunet et al., 1999; Henderson & Johnson, 2001; Lin et al., 2001; Calnan & Brunet, 2008; Zanella et al., 2010; Webb & Brunet, 2014).”
- Redox regulation of FoxO transcription factors (2015, background): “This switch may allow cells to survive oxidative and metabolic stresses, as it has been demonstrated for FoxO3a in the landmark study by Brunet et al. [101].”
- ER stress: Autophagy induction, inhibition and selection (2015, background): “These pathways regulate the subcellular localization, protein level, DNA binding, and transcriptional properties of FOXO.(196) The C-terminal DNA binding domain of FOXO proteins possesses both the nuclear localization and nuclear export sequences.”
- mTOR signaling at a glance (2009, background): “…mTORC2 depletion reduces the phosphorylation of, and therefore activates, the forkhead box protein O1 (FoxO1) and FoxO3a transcription factors, which control the expression of genes involved in stress resistance, metabolism, cell-cycle arrest and apoptosis (reviewed by Calnan and Brunet, 2008).”
- The NAD+ precursor nicotinamide riboside enhances oxidative metabolism and protects against high-fat diet induced obesity (2012, positive): “This deacetylation of FOXO1 by SIRT1 upon NR treatment resulted in its transcriptional activation, leading to higher expression of target genes, such as Gadd45, Catalase, Sod1, and Sod2 (see Figure S1 online) (Calnan and Brunet, 2008).”