Curated Information
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PubMed Id: 17349958 
Taira N, et al. (2007) DYRK2 is targeted to the nucleus and controls p53 via Ser46 phosphorylation in the apoptotic response to DNA damage. Mol Cell 25, 725-38 17349958
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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S46-p - p53 (human)
Orthologous residues
p53 (human): S46‑p, p53 (mouse): L43‑p, p53 iso2 (mouse): L46‑p, p53 (rat): L48‑p, p53 (rabbit): S45‑p, p53 (monkey): S46‑p
 Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  bone cancer, colorectal cancer, colorectal carcinoma
 Relevant cell lines - cell types - tissues:  293T (epithelial), HCT116 (intestinal), Saos-2 (bone cell), SW480 (intestinal), U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE DYRK2 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE DYRK2 (human) co-immunoprecipitation, transfection of inactive enzyme, pharmacological activator of upstream enzyme, phospho-antibody, siRNA inhibition of enzyme, microscopy-colocalization, transfection of wild-type enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
adriamycin ATM (human) increase ATM siRNA inhibits adriamycin response
UV increase
Downstream Regulation
 Effect of modification (process):  apoptosis, induced

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