Curated Information
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Curated Information Page
PubMed Id: 19122209 
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.
Chiba S, Tokuhara M, Morita EH, Abe S (2009) TTP at Ser245 phosphorylation by AKT is required for binding to 14-3-3. J Biochem 145, 403-9 19122209
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S245-p - SH3BP4 (mouse)
Orthologous residues
SH3BP4 (human): S246‑p, SH3BP4 (mouse): S245‑p, SH3BP4 (rat): S244‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site
 Relevant cell lines - cell types - tissues:  CHO-K1 (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  hamster
 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, modification site within consensus motif
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
H2O2 increase
Akt inhibitor VIII H2O2 inhibit treatment-induced 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 (mouse) Induces co-immunoprecipitation


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