FoxO1 protects against pancreatic beta cell failure through NeuroD and MafA induction.

By Y. Kitamura, T. Kitamura, J. Kruse, Jeffrey C. Raum, R. Stein, W. Gu, D. Accili. Cell Metabolism, 2005

601 citations recorded by the source corpus.

Subfields: Geriatrics and Gerontology, Molecular Biology, Surgery

View Paper: https://www.semanticscholar.org/paper/e547d04635490cf51a382fd7b5c4e80f1a0ace06

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Geriatrics and Gerontology

1. Johan Auwerx
2. D. Sinclair
3. L. Guarente
4. M. Haigis
5. C. Cantó
6. R. Houtkooper
7. R. Mostoslavsky
8. W. Gu

In Molecular Biology

1. L. Guarente
2. W. Gu
3. Johan Auwerx
4. D. Sinclair
5. R. Houtkooper
6. M. Haigis
7. R. Mostoslavsky
8. C. Cantó

In Surgery

1. C. Cantó
2. Johan Auwerx
3. D. Accili
4. J. Y. Chiang

Citations in the corpus

• SIRT4 inhibits glutamate dehydrogenase and opposes the effects of calorie restriction in pancreatic beta cells. (2006, background): “SIRT1 deacetylates the forkhead transcription factor FOXO1 (Brunet et al., 2004; Luo et al., 2001; Motta et al., 2004; Vaziri et al., 2001) and thereby promotes resistance to Cell 126, 941–954, September 8, 2006 ª2006 Elsevier Inc. 941 oxidative stress in b cells (Kitamura et al., 2005).”
• The role of FoxO in the regulation of metabolism (2008, background): “However, it also helps to preserve beta cell function under conditions of oxidative stress, such as in insulin-resistant states (Kitamura et al., 2005).”
• The secret life of NAD+: an old metabolite controlling new metabolic signaling pathways. (2010, background): “Additionally, SIRT1 action prevents oxidative damage in the pancreas, not only by decreasing the production of reactive oxygen species in the mitochondria, but also by enhancing FOXO and PGC-1 -mediated transcription of detoxification genes (111, 112).”
• Cytosolic FoxO1 is essential for the induction of autophagy and tumour suppressor activity (2010, background): “However, the phosphorylation status and subcellular localization of FoxO1 depend on the stimul”
• SIRTUIN 1 AND SIRTUIN 3: PHYSIOLOGICAL MODULATORS OF METABOLISM (2012, background): “In the hyperglycemic state, oxidative stress can induce pancreatic beta cell failure (175).”
• Mammalian sirtuins--emerging roles in physiology, aging, and calorie restriction. (2006, background): “The yeast ortholog of SIRT2, Hst2, can function in parallel to SIR2 in certain strains with respect to lifespan extension and rDNA silencing (Lamming et al. 2005).”
• Pancreatic β-Cell Dedifferentiation As Mechanism Of Diabetic β-Cell Failure (2012, neutral): “, 2010), by suggesting that plasticity occurs in common forms of b cell dysfunction, and is caused by the downregulation of FoxO1 that follows hyperglycemia-induced oxidative stress (Kitamura et al., 2005).”
• Brown Remodeling of White Adipose Tissue by SirT1-Dependent Deacetylation of Pparγ (2012, neutral): “HA-Pparg (Kitamura et al., 2005) and SirT1 adenoviruses have been described (Nakae et al.”
• Glucose restriction inhibits skeletal myoblast differentiation by activating SIRT1 through AMPK-mediated regulation of Nampt. (2008, background): “, 2004) and pancreatic β-cells (Kitamura et al., 2005), insulin secretion (Bordone et al.”
• Redox regulation of FoxO transcription factors (2015, background): “As deacetylated FoxOs are then again more sensitive to poly-ubiquitination and proteasomal degradation [116,128], the (de)acetylation-mediated switch in gene expression of FoxO target genes is expected to protect cells from acute but not from chronic stress.”
• Hepatocyte-specific Deletion of SIRT1 Alters Fatty Acid Metabolism and Results in Hepatic Steatosis and Inflammation (2009, background): “This mechanism has been well described for other SIRT1-mediated transcriptional activations (Kitamura et al., 2005; Li et al., 2007; Pagans et al., 2005).”