Curated Information
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Curated Information Page
PubMed Id: 20629186 
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.
Urano-Tashiro Y, et al. (2010) Implication of Akt-dependent Prp19 alpha/14-3-3beta/Cdc5L complex formation in neuronal differentiation. J Neurosci Res 88, 2787-97 20629186
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T193-p - PRPF19 (human)
Orthologous residues
PRPF19 (human): T193‑p, PRPF19 (mouse): T193‑p, PRPF19 (rat): T193‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site
 Disease tissue studied:  adrenal cancer, pheochromocytoma
 Relevant cell lines - cell types - tissues:  COS (fibroblast), PC-12 (chromaffin)
 Cellular systems studied:  cell lines
 Species studied:  monkey
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Akt1 (rat) pharmacological activator of upstream enzyme, modification site within consensus motif, activation of upstream enzyme, pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
EGF increase
wortmannin EGF inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (function):  intracellular localization, 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, yeast two-hybrid
CDC5L (mouse) Induces co-immunoprecipitation
 Comments:  involved in neuronal differentiation


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