Curated Information
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Curated Information Page
PubMed Id: 17540171 
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.
Liu B, et al. (2007) Proinflammatory stimuli induce IKKalpha-mediated phosphorylation of PIAS1 to restrict inflammation and immunity. Cell 129, 903-14 17540171
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S90-p - PIAS1 (mouse)
Orthologous residues
PIAS1 (human): S90‑p, PIAS1 (mouse): S90‑p, PIAS1 (rat): S90‑p
Characterization
 Methods used to characterize site in vivo [32P] bio-synthetic labeling, mass spectrometry, mutation of modification site, phospho-antibody
 Relevant cell lines - cell types - tissues:  293T (epithelial), macrophage-bone marrow, MEF (fibroblast) [IGF1R (mouse)], RAW 264 (macrophage), splenocyte
 Cellular systems studied:  cell lines, primary cultured cells
 Species studied:  human, mouse
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE IKKA (human) siRNA inhibition of enzyme, genetic knockout/knockin of upstream enzyme, co-immunoprecipitation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
UV increase
TNF increase
LPS increase
IFN-gamma increase
anti-CD3/CD28 increase
Downstream Regulation
 Effect of modification (process):  transcription, inhibited
 Comments:  phosphorylation of this site inhibits TNF-induced expression of NFKB-target genes and IFN-induced expression of STAT1-target genes;


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