Curated Information
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Curated Information Page
PubMed Id: 12808093 
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.
Trencia A, et al. (2003) Protein kinase B/Akt binds and phosphorylates PED/PEA-15, stabilizing its antiapoptotic action. Mol Cell Biol 23, 4511-21 12808093
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S116-p - PEA-15 (human)
Orthologous residues
PEA‑15 (human): S116‑p, PEA‑15 (mouse): S116‑p, PEA‑15 (rat): S116‑p, PEA‑15 (hamster): S116‑p
Characterization
 Methods used to characterize site in vivo [32P] bio-synthetic labeling, immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  brain cancer, glioblastoma, glioblastoma multiforme, glioma
 Relevant cell lines - cell types - tissues:  293 (epithelial), U373 MG (glial)
 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) co-immunoprecipitation, transfection of constitutively active enzyme, transfection of wild-type enzyme, transfection of inactive enzyme, pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
serum increase
wortmannin serum inhibit treatment-induced increase
insulin increase
wortmannin insulin inhibit treatment-induced increase
KN-93 insulin no effect upon treatment-induced increase
bisindolylmaleimide insulin no effect upon treatment-induced increase
Downstream Regulation
 Effect of modification (function):  protein stabilization
 Effect of modification (process):  apoptosis, inhibited


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