Curated Information
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Curated Information Page
PubMed Id: 16505154 
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.
Hao Q, Rutherford SA, Low B, Tang H (2006) Suppression of the phosphorylation of receptor tyrosine phosphatase-alpha on the Src-independent site tyrosine 789 by reactive oxygen species. Mol Pharmacol 69, 1938-44 16505154
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Y789-p - PTPRA iso2 (human) ▲
Orthologous residues
PTPRA (human): Y798‑p, PTPRA iso2 (human): Y789‑p, PTPRA (mouse): Y825‑p, PTPRA (rat): Y792‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  293 (epithelial), endothelial-aorta, HUVEC (endothelial), MEF (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
H2O2 inhibit treatment-induced decrease H2O2 inhibits ST789 phosphorylation in various cell lines and is dose-dependent.
GF109203X, rottlerin, BAPTA-AM, PP1 H2O2 augment treatment-induced decrease PP1 and other inhibitors inhibit T789 phosphorylation alone and when treated with H2O2.


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