Curated Information
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Curated Information Page
PubMed Id: 10102273 
Brunet A, et al. (1999) Akt promotes cell survival by phosphorylating and inhibiting a Forkhead transcription factor. Cell 96, 857-68 10102273
This page summarizes selected information from the record referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2015, 43:D512-20). To learn more about the scope of PhosphoSitePlus®, click here.
Click on the protein name to open the protein page, and on the RSD number to open the site page.
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S253-p - FOXO3A (human) ▲
Modsite: APRRRAVsMDNSNkY SwissProt Entrez-Gene
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) ▲
Modsite: DFRsRTNsNAstVsG SwissProt Entrez-Gene
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) ▲
Modsite: QSRPRSCtWPLQRPE SwissProt Entrez-Gene
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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