Curated Information
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Curated Information Page
PubMed Id: 16873060 
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.
Scaglioni PP, et al. (2006) A CK2-dependent mechanism for degradation of the PML tumor suppressor. Cell 126, 269-83 16873060
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S565-p - PML (human)
Orthologous residues
PML (human): S565‑p, PML iso2 (human): S565‑p, PML iso3 (human): S565‑p, PML iso4 (human): , PML iso10 (human): , PML iso11 (human): S517‑p, PML iso14 (human): , PML (mouse): S575‑p, PML iso2 (mouse): S529‑p, PML (rat): S563‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  colorectal cancer, colorectal carcinoma
 Relevant cell lines - cell types - tissues:  293 (epithelial), 3T3 (fibroblast), Colo-320 (intestinal), MEF (fibroblast), WI-38 (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE CK2A1 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE CK2A1 (human) pharmacological activator of upstream enzyme, microscopy-colocalization, phospho-antibody, modification site within consensus motif, pharmacological inhibitor of upstream enzyme, siRNA inhibition of enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
osmotic stress increase
UV increase
TBB UV inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (function):  protein degradation
 Effect of modification (process):  apoptosis, inhibited, cell growth, altered


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