Curated Information
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PubMed Id: 12000790 
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.
Information from this record has been curated, but not yet edited in PhosphoSitePlus® and may be incomplete.
Amit S, et al. (2002) Axin-mediated CKI phosphorylation of beta-catenin at Ser 45: a molecular switch for the Wnt pathway. Genes Dev 16, 1066-76 12000790
Only sites from this record are displayed on this page. Click on the protein name to open the protein page, and on the RSD number to open the site page. For the complete dataset, click the download button, on the right.
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S33-p - CTNNB1 (human) ▲
Orthologous residues
CTNNB1 (human): S33‑p, CTNNB1 (mouse): S33‑p, CTNNB1 (rat): S33‑p
Characterization
 Methods used to characterize site in vivo:  mass spectrometry, mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  293 (epithelial), HeLa (cervical), Jurkat (T lymphocyte), L cells (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE GSK3B (human)
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
lithium decrease
CK1-7 decrease
H-89 no change compared to control
axin 1 (human) increase
Wnt3a decrease
Downstream Regulation
 Effect of modification (function):  protein degradation

S37-p - CTNNB1 (human) ▲
Orthologous residues
CTNNB1 (human): S37‑p, CTNNB1 (mouse): S37‑p, CTNNB1 (rat): S37‑p
Characterization
 Methods used to characterize site in vivo:  mass spectrometry, mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  293 (epithelial), HeLa (cervical), Jurkat (T lymphocyte), L cells (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE GSK3B (human)
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
lithium decrease
CK1-7 decrease
H-89 no change compared to control
axin 1 (human) increase
Downstream Regulation
 Effect of modification (function):  protein degradation

T41-p - CTNNB1 (human) ▲
Orthologous residues
CTNNB1 (human): T41‑p, CTNNB1 (mouse): T41‑p, CTNNB1 (rat): T41‑p
Characterization
 Methods used to characterize site in vivo:  mass spectrometry, mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  293 (epithelial), HeLa (cervical), Jurkat (T lymphocyte), L cells (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE GSK3B (human)
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
CK1-7 decrease
H-89 no change compared to control
lithium no change compared to control
axin 1 (human) increase
Wnt3a decrease
Downstream Regulation
 Effect of modification (function):  protein degradation

S45-p - CTNNB1 (human) ▲
Orthologous residues
CTNNB1 (human): S45‑p, CTNNB1 (mouse): S45‑p, CTNNB1 (rat): S45‑p
Characterization
 Methods used to characterize site in vivo:  mass spectrometry, mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  293 (epithelial), HeLa (cervical), Jurkat (T lymphocyte), L cells (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE CK1-D (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE CK1-E (human) pharmacological activator of upstream enzyme, transfection of wild-type enzyme, phospho-antibody, pharmacological inhibitor of upstream enzyme, transfection of dominant-negative enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
CK1-7 decrease
H-89 no change compared to control
lithium no change compared to control
axin 1 (human) increase
Wnt3a decrease
Downstream Regulation
 Effect of modification (function):  phosphorylation, protein degradation
 Comments:  priming phosphorylation for T41/S37/S33


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