Curated Information
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Curated Information Page
PubMed Id: 20629186 
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
This page summarizes selected information from the record 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.
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T193-p - PRPF19 (human)
Orthologous residues
PRPF19 (human): T193‑p, PRPF19 (mouse): T193‑p, PRPF19 (rat): T193‑p
 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 inhibitor of upstream enzyme, activation of upstream enzyme, pharmacological activator 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
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
CDC5L (mouse) Induces co-immunoprecipitation
14-3-3 beta (mouse) Induces co-immunoprecipitation, yeast two-hybrid
 Comments:  involved in neuronal differentiation

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