Curated Information
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PubMed Id: 10358075 
Rena G, et al. (1999) Phosphorylation of the transcription factor forkhead family member FKHR by protein kinase B. J Biol Chem 274, 17179-83 10358075
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, 2012,40:D261-70). To learn more about the scope of PhosphoSitePlus®, click here.
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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T24-p - FOXO1A (human)
Orthologous residues
FOXO1A (human): T24‑p, FOXO1A (mouse): T24‑p, FOXO1A (rat): T24‑p
Characterization
 Methods used to characterize site in vivo phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  293 (epithelial)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE Akt1 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Akt1 (human) pharmacological inhibitor of upstream enzyme, activation of upstream enzyme, pharmacological activator of upstream enzyme, phospho-antibody, genetic transfer of constitutively active upstream enzyme kinase activation = transfection of PDK1 (upstream activator of Akt1)
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
Akt1 (human) increase constitutively active AKT
PDK1 (human) increase
IGF-1 increase
wortmannin IGF-1 inhibit treatment-induced increase
PD98059 IGF-1 no effect upon treatment-induced increase
rapamycin IGF-1 no effect upon treatment-induced increase

S256-p - FOXO1A (human)
Orthologous residues
FOXO1A (human): S256‑p, FOXO1A (mouse): S253‑p, FOXO1A (rat): S250‑p
Characterization
 Methods used to characterize site in vivo phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  293 (epithelial)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE Akt1 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Akt1 (human) pharmacological inhibitor of upstream enzyme, activation of upstream enzyme, pharmacological activator of upstream enzyme, phospho-antibody, genetic transfer of constitutively active upstream enzyme kinase activation = transfection of PDK1 (upstream activator of Akt1)
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
Akt1 (human) increase constitutively active AKT
PDK1 (human) increase
IGF-1 increase
wortmannin IGF-1 inhibit treatment-induced increase
PD98059 IGF-1 no effect upon treatment-induced increase
rapamycin IGF-1 no effect upon treatment-induced increase

S319-p - FOXO1A (human)
Orthologous residues
FOXO1A (human): S319‑p, FOXO1A (mouse): S316‑p, FOXO1A (rat): S313‑p
Characterization
 Methods used to characterize site in vivo phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  293 (epithelial)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE Akt1 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Akt1 (human) pharmacological inhibitor of upstream enzyme, activation of upstream enzyme, pharmacological activator of upstream enzyme, phospho-antibody, genetic transfer of constitutively active upstream enzyme kinase activation = transfection of PDK1 (upstream activator of Akt1)
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
Akt1 (human) increase constitutively active AKT
PDK1 (human) increase
IGF-1 increase
wortmannin IGF-1 inhibit treatment-induced increase
PD98059 IGF-1 no effect upon treatment-induced increase
rapamycin IGF-1 no effect upon treatment-induced increase


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