Curated Information
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Curated Information Page
PubMed Id: 17349958 
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.
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
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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
Characterization
 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) transfection of wild-type enzyme, pharmacological activator of upstream enzyme, phospho-antibody, microscopy-colocalization, siRNA inhibition of enzyme, transfection of inactive enzyme, co-immunoprecipitation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
adriamycin increase
siRNA adriamycin ATM (human) inhibit treatment-induced increase
UV increase
Downstream Regulation
 Effect of modification (process):  apoptosis, induced


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