Curated Information
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Curated Information Page
PubMed Id: 17998334 
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.
Johnstone CN, et al. (2008) Parvin-beta inhibits breast cancer tumorigenicity and promotes CDK9-mediated peroxisome proliferator-activated receptor gamma 1 phosphorylation. Mol Cell Biol 28, 687-704 17998334
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S112-p - PPAR-gamma (human)
Orthologous residues
PPAR‑gamma (human): S112‑p, PPAR‑gamma iso3 (human): S84‑p, PPAR‑gamma (mouse): S112‑p, PPAR‑gamma iso2 (mouse): S82‑p, PPAR‑gamma (rat): S112‑p
Characterization
 Methods used to characterize site in vivo phospho-antibody, western blotting
 Disease tissue studied:  breast cancer
 Relevant cell lines - cell types - tissues:  MDA-MB231 (breast cell)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE CDK9 (human) siRNA inhibition of enzyme, phospho-antibody, pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
PARVB (human) increase
rosiglitazone PARVB (human) no effect upon treatment-induced increase
DRB PARVB (human) inhibit treatment-induced increase
rosiglitazone no change compared to control
DRB decrease


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