Curated Information
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Curated Information Page
PubMed Id: 17277771 
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.
Information from this record has been curated, but not yet edited in PhosphoSitePlus® and may be incomplete.
Vander Haar E, et al. (2007) Insulin signalling to mTOR mediated by the Akt/PKB substrate PRAS40. Nat Cell Biol 9, 316-23 17277771
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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S473-p - Akt1 (human) ▲
Orthologous residues
Akt1 (human): S473‑p, Akt1 (mouse): S473‑p, Akt1 (rat): S473‑p, Akt1 (fruit fly): S586‑p, Akt1 (cow): S473‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  3T3-L1 (fibroblast), HepG2 (hepatic)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
insulin increase
wortmannin insulin inhibit treatment-induced increase

S636-p - IRS1 (human) ▲
Orthologous residues
IRS1 (human): S636‑p, IRS1 (mouse): S632‑p, IRS1 (rat): S632‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  3T3-L1 (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  mouse

S639-p - IRS1 (human) ▲
Orthologous residues
IRS1 (human): S639‑p, IRS1 (mouse): S635‑p, IRS1 (rat): S635‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  3T3-L1 (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  mouse

T412-p - p70S6K (human) ▲
Orthologous residues
p70S6K (human): T412‑p, p70S6K iso2 (human): T389‑p, p70S6K (mouse): T412‑p, p70S6K (rat): T412‑p, p70S6K iso2 (rat): T389‑p, p70S6K (fruit fly): T398‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  3T3-L1 (fibroblast), HepG2 (hepatic)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
amino acid starvation decrease
insulin increase
wortmannin insulin inhibit treatment-induced increase

T246-p - PRAS40 (human) ▲
Orthologous residues
PRAS40 (human): T246‑p, PRAS40 iso3 (human): T266‑p, PRAS40 (mouse): T247‑p, PRAS40 (rat): T247‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  293T (epithelial), 3T3-L1 (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Akt1 (human) pharmacological inhibitor of upstream enzyme, modification site within consensus motif, phospho-antibody, transfection of wild-type enzyme, pharmacological activator of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
insulin increase
wortmannin insulin inhibit treatment-induced increase
amino acid starvation increase
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
14-3-3 beta (human) Induces molecular association, regulation co-immunoprecipitation


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