Curated Information
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Curated Information Page
PubMed Id: 11438550 
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.
Masuyama N, et al. (2001) Akt inhibits the orphan nuclear receptor Nur77 and T-cell apoptosis. J Biol Chem 276, 32799-805 11438550
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S350-p - Nur77 (rat)
Orthologous residues
Nur77 (human): S351‑p, Nur77 (mouse): S354‑p, Nur77 (rat): S350‑p
Characterization
 Methods used to characterize site in vivo electrophoretic mobility shift, mutation of modification site, phospho-antibody
 Relevant cell lines - cell types - tissues:  293T (epithelial) [Akt1 (human)], 293T (epithelial) [Nur77 (rat)]
 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) transfection of constitutively active enzyme
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Effect of modification (process):  apoptosis, inhibited
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
14-3-3 beta (rat) Induces co-immunoprecipitation


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