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©2014 Baishideng Publishing Group Inc.
World J Biol Chem. Aug 26, 2014; 5(3): 346-354
Published online Aug 26, 2014. doi: 10.4331/wjbc.v5.i3.346
Published online Aug 26, 2014. doi: 10.4331/wjbc.v5.i3.346
Figure 2 Major phosphorylation and acetylation residues of FoxO3a.
Post-translational modification sites of FoxO3a. Shown are sites of serine/threonine phosphorylation by Akt/SGK, MST1, IKKβ or the residues acetylated by CBP or unidentified acetyl transferases (?) on FoxO3a domains[12]. FKH: Forkhead DNA binding domain; NLS: Nuclear localization signal; NES: Nuclear export sequence; TA: Transactivation domain; Akt: Protein kinase B; MST1: Mammalian sterile 20 like kinase-1; CBP: The cyclic–AMP responsive element binding (CREB) binding protein, IKKβ: Ikβ kinase; SGK: Serum-and glucocorticoid-induced protein kinase.
- Citation: Nho RS, Hergert P. FoxO3a and disease progression. World J Biol Chem 2014; 5(3): 346-354
- URL: https://www.wjgnet.com/1949-8454/full/v5/i3/346.htm
- DOI: https://dx.doi.org/10.4331/wjbc.v5.i3.346