Table 1.
Cellular output | Gene | Function | Regulation in cells | Binding to promoter | Regulation of promoter | References |
---|---|---|---|---|---|---|
Metabolism | G6pc | glycogenolysis | + | EMSA | + | [19,29,57] |
Igfbp1 | regulates IGF activity | + | ChIP | + | [27,57,58,59] | |
Ppargc1 α | gluconeogenesis | + | [57] | |||
Pck1 | gluconeogenesis | + | EMSA | + | [57,58] | |
Food intake | Agrp | orexigenic neuropeptide | + | ChIP; EMSA | + | [61,62] |
Npy | orexigenic neuropeptide | + | ChIP; EMSA | + | [61] | |
Pomc | anorexigenic neuropeptide | - | ChIP; EMSA | + | [61,62] | |
Atrophy | Atrogin-1/MAFbx | muscle-specific ubiquitin ligase | + | EMSA | + | [66,67] |
MuRF1 | muscle-specific ubiquitin ligase | + | [66] | |||
Autophagy | Bnip3 | Bcl2-related autophagy regulator | + | ChIP | [21,70] | |
Gabarapl1 | autophagosome formation | + | ChIP | [72] | ||
LC3 | autophagosome formation | + | ChIP | + | [70,72] | |
Atg12I | autophagy-related gene | + | ChIP | [72] | ||
Apoptosis | Bim | Bcl2-interacting mediator of cell death | + | ChIP | + | [15,28,75] |
hid | pro-apoptotic | + | ChIP | [76] | ||
Fas ligand | pro-apoptotic tumor necrosis factor ligand | + | [1] | |||
Cell cycle arrest | p27Kip1 | binds to and inhibits the cyclin E–CDK2 complex | + | + | [18,82] | |
p21Cip1 | binds to and inhibits the cyclin E–CDK2 complex | + | ChIP | + | [30,34] | |
p19INK4d p19Arf | binds to and inhibits cyclin D–CDK4/6 complexes | + | ChIP; EMSA | + | [32,83] | |
p15INK4b | binds to and inhibits cyclin D–CDK4/6 complexes | + | ChIP; EMSA | + | [32,33,34] | |
Angiogenesis | Sprouty2 | inhibitor of tyrosine kinase signaling | + | ChIP | [63] | |
eNOS | endothelial function and neovascularization | - | ChIP | + | [64] | |
Ang2 | vascular remodelling factor | + | [64] | |||
Cited2 | CBP/p300-interacting transactivator | + | ChIP | + | [38,63] | |
Stress resistance | MnSOD | manganese superoxide dismutase | + | ChIP | + | [20,82] |
Gadd45α | growth arrest- and DNA damage-inducible gene 45 α | + | + | [21] |
Footnotes
The list of target genes is not exhaustive.
Regulation in cells details whether FoxO factors promote (+) or suppress (-) target gene expression in cultured cells by assessment of mRNA or protein levels.
Direct binding of FoxO factors to the promoter was assessed by chromatin immunoprecipitation (ChIP) or electromobility shift assay (EMSA).
Regulation of promoters was tested by the ability of FoxO factors to specifically drive luciferase expression.