The forkhead transcription factor Foxo1 (Fkhr) confers insulin sensitivity onto glucose-6-phosphatase expression.
By Jun Nakae, T. Kitamura, David L. Silver, Domenico Accili. Journal of Clinical Investigation, 2001
612 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/9ba374eb49e25d1e54d71b5dc03f6c980a1d97c1
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Citations in the corpus
- Impaired regulation of hepatic glucose production in mice lacking the forkhead transcription factor Foxo1 in liver. (2007, background): “Although we have previously shown that Foxo1 plays a role in insulin inhibition of cAMPinduced glucose production (Nakae et al., 2001; Puig- 214 Cell Metabolism 6, 208–216, September 2007 ª2007 Els server et al., 2003), the present data show that it is required for cAMP induction of HGP, thus…”
- mTOR: from growth signal integration to cancer, diabetes and ageing (2010, background): “When glucose is abundant, insulin signalling through Akt suppresses the expression of phosphoenolpyruvate carboxykinase (PEPCK), a transcriptional target of FOXO1 that is the limiting enzyme of gluconeogenesis in the live”
- Regulation of insulin action and pancreatic β-cell function by mutated alleles of the gene encoding forkhead transcription factor Foxo1 (2002, background): “Our genetic analysis supports the idea that Foxo1 acts in insulin regulation of G6pc, which effects the rate-limiting step in the conversion of glucose-6-phosphate to glucose that controls hepatic and renal glucose outpu”
- Control of cell number by Drosophila FOXO: downstream and feedback regulation of the insulin receptor pathway. (2003, background): “2000) and modulate metabolic genes (Ayala et al. 1999; Durham et al. 1999; Guo et al. 1999; Hall et al. 2000; Nasrin et al. 2000; Schmoll et al. 2000; Nakae et al. 2001; Nadal et al. 2002).”
- FOXO transcription factors directly activate bim gene expression and promote apoptosis in sympathetic neurons (2003, methodology): “The FKHR(ADA) adenovirus (Ad-ADA-Foxo1; provided by D. Accili, Columbia University, New York, NY) and the LacZ adenovirus have been described previously (Nakae et al., 2001; Whitfield et al., 2001).”
- Mammalian SIRT1 represses forkhead transcription factors. (2004, background): “Other genes activated by Foxo in mammals, such as PEPCK, control the gluconeogenic pathway that drives the production of glucose in the liver upon starvation (Daitoku et al., 2003; Barthel et al., 2001; Nakae et al., 2001).”
- 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].”
- Mechanisms and disease consequences of nonalcoholic fatty liver disease (2021, background): “Although insulin can also regulate hepatic gluconeogenesis through FOXO1mediated transcriptional/translational events, these effects do not occur acutely andmore likely set the capacity for hepatic gluconeogenic flux.”
- Non-Alcoholic Fatty Liver Disease as a Nexus of Metabolic and Hepatic Diseases (2017, positive): “, 1998b) and (2) lowering expression of gluconeogenic enzymes via phosphorylation and nuclear exclusion of FOXO1 (Nakae et al., 2001).”