SIRT2 deacetylates FOXO3a in response to oxidative stress and caloric restriction

By Fei Wang, Margaret Nguyen, F. Xiao‐Feng Qin, Q. Tong. Aging Cell, 2007

648 citations recorded by the source corpus.

How researchers see this paper

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

Redox regulation of FoxO transcription factors (2015, background): “It has been shown that the cytosolic isoform Sirt2 is capable of deacetylating FoxO1a and FoxO3a, thereby promoting their re-localization from the cytoplasm to the nucleus and increasing FoxO-dependent transcription of antioxidant enzymes [134,135].”
FoxOs cooperatively regulate diverse pathways governing neural stem cell homeostasis (2009, background): “…observations including cell cycle (e.g., G two and S phase expressed1, Cdk inhibitor 1C, Sal like2) and glial differentiation (e.g., Hes5, Sox10, Myelin basic protein, Plp1, Cystatin C) and that functionally interact with FoxOs (e.g., FoxG1, Sirt2) (Seoane et al., 2004; Wang et al., 2007).”
The Role of Sirtuins in Antioxidant and Redox Signaling (2017, background): “SIRT2 has also been shown to deacetylate FOXO3a in response to oxidative stress, which is helpful because FOXO3a is a transcriptional activator of the SOD2 gene that encodes MnSOD protein, a powerful antioxidant (168).”