Curated Information
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Curated Information Page
PubMed Id: 11551930 
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.
Xie S, et al. (2001) Plk3 functionally links DNA damage to cell cycle arrest and apoptosis at least in part via the p53 pathway. J Biol Chem 276, 43305-12 11551930
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S20-p - p53 (human)
Orthologous residues
p53 (human): S20‑p, p53 (mouse): S20‑p, p53 iso2 (mouse): S23‑p, p53 (rat): S20‑p, p53 (rabbit): S20‑p, p53 (monkey): S20‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  GM00637 (fibroblast), HeLa (cervical)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE PLK3 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PLK3 (human) transfection of dominant-negative enzyme, pharmacological activator of upstream enzyme, phospho-antibody, co-immunoprecipitation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
adriamycin increase
Downstream Regulation
 Effect of modification (process):  cell growth, altered, transcription, altered


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