Curated Information
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Curated Information Page
PubMed Id: 17237784 
He XC, et al. (2007) PTEN-deficient intestinal stem cells initiate intestinal polyposis. Nat Genet 39, 189-98 17237784
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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S552-p - CTNNB1 (mouse)
Orthologous residues
CTNNB1 (human): S552‑p, CTNNB1 (mouse): S552‑p, CTNNB1 (rat): S552‑p
 Methods used to characterize site in vivo immunoprecipitation, phospho-antibody
 Disease tissue studied:  Cowden disease
 Relevant cell lines - cell types - tissues:  intestine
 Cellular systems studied:  tissue
 Species studied:  mouse
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE Akt1 (human)
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
PTEN (mouse) decrease increased in PTEN -/- mouse; associated with increased intestinal polyposis
Downstream Regulation
 Effect of modification (function):  intracellular localization
Associated Diseases
Diseases: Alterations: Comments:
Cowden disease increased observed in PTEN mouse mutant

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