Curated Information
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Curated Information Page
PubMed Id: 10102273 
This page summarizes selected information from the article referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2012,40:D261-70). To learn more about the scope of PhosphoSitePlus®, click here.
Brunet A, et al. (1999) Akt promotes cell survival by phosphorylating and inhibiting a Forkhead transcription factor. Cell 96, 857-68 10102273
Only sites from this record are displayed on this page. Click on the protein name to open the protein page, and on the RSD number to open the site page. For the complete dataset, click the download button, on the right.
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S253-p - FOXO3A (human) ▲
Orthologous residues
FOXO3A (human): S253‑p, FOXO3A (mouse): S252‑p, FOXO3A (rat): S252‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  'neuron, cerebellar granule'-brain, 293T (epithelial), CCL39 (fibroblast)
 Cellular systems studied:  cell lines, primary cultured cells
 Species studied:  hamster, human, rat
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE Akt1 (mouse)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Akt1 (human) genetic transfer of constitutively active upstream enzyme, pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
IGF-1 increase
LY294002 IGF-1 inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (function):  intracellular localization, molecular association, regulation
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
14-3-3 zeta (mouse) Induces co-immunoprecipitation

S315-p - FOXO3A (human) ▲
Orthologous residues
FOXO3A (human): S315‑p, FOXO3A (mouse): S314‑p, FOXO3A (rat): S314‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  'neuron, cerebellar granule'-brain, 293T (epithelial), CCL39 (fibroblast)
 Cellular systems studied:  cell lines, primary cultured cells
 Species studied:  hamster, human, rat
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
IGF-1 increase
LY294002 IGF-1 inhibit treatment-induced increase

T32-p - FOXO3A (mouse) ▲
Orthologous residues
FOXO3A (human): T32‑p, FOXO3A (mouse): T32‑p, FOXO3A (rat): T32‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  'neuron, cerebellar granule'-brain, 293T (epithelial), CCL39 (fibroblast)
 Cellular systems studied:  cell lines, primary cultured cells
 Species studied:  hamster, human, rat
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE Akt1 (mouse)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Akt1 (human) genetic transfer of constitutively active upstream enzyme, pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
IGF-1 increase
LY294002 IGF-1 inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (function):  intracellular localization, molecular association, regulation
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
14-3-3 zeta (mouse) Induces co-immunoprecipitation


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