Curated Information
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Curated Information Page
PubMed Id: 17177604 
Gherzi R, et al. (2006) The RNA-binding protein KSRP promotes decay of beta-catenin mRNA and is inactivated by PI3K-AKT signaling. PLoS Biol 5, e5 17177604
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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S193-p - KHSRP (human)
Orthologous residues
KHSRP (human): S193‑p, KHSRP (mouse): S194‑p, KHSRP (rat): S194‑p
Characterization
 Methods used to characterize site in vivo [32P] bio-synthetic labeling, immunoprecipitation, mutation of modification site
 Relevant cell lines - cell types - tissues:  293T (epithelial), HeLa (cervical)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE Akt2 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Akt1 (human) transfection of wild-type enzyme
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Effect of modification (process):  transcription, altered
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
14-3-3 zeta (human) Induces transcription, altered co-immunoprecipitation, pull-down assay
 Comments:  controls beta-catenin gene expression by controlling its mRNA stability; phosphorylation of this site inhibits interaction with the exosome


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