Curated Information
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Curated Information Page
PubMed Id: 20101225 
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.
He X, et al. (2010) c-Abl regulates estrogen receptor alpha transcription activity through its stabilization by phosphorylation. Oncogene 29, 2238-51 20101225
Only sites from this record are displayed on this page. Click on the protein name to open the protein page, and on the RSD number to open the site page. For the complete dataset, click the download button, on the right.
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Y52-p - ER-alpha (human)
Orthologous residues
ER‑alpha (human): Y52‑p, ER‑alpha (mouse): F52‑p, ER‑alpha (rat): F52‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  breast cancer
 Relevant cell lines - cell types - tissues:  293 (epithelial), MCF-7 (breast cell), ZR-75-1 (breast cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE Abl (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Abl (human) modification site within consensus motif, pharmacological inhibitor of upstream enzyme, siRNA inhibition of enzyme, transfection of wild-type enzyme, co-immunoprecipitation, transfection of inactive enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
STI571 decrease
Downstream Regulation
 Effect of modification (function):  protein stabilization
 Effect of modification (process):  carcinogenesis, induced, cell growth, induced, transcription, induced
Associated Diseases
Diseases: Alterations: Comments:
breast cancer increased

Y219-p - ER-alpha (human)
Orthologous residues
ER‑alpha (human): Y219‑p, ER‑alpha (mouse): Y223‑p, ER‑alpha (rat): Y224‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  breast cancer
 Relevant cell lines - cell types - tissues:  293 (epithelial), MCF-7 (breast cell), ZR-75-1 (breast cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE Abl (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Abl (human) modification site within consensus motif, pharmacological inhibitor of upstream enzyme, siRNA inhibition of enzyme, transfection of wild-type enzyme, co-immunoprecipitation, transfection of inactive enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
STI571 decrease
Downstream Regulation
 Effect of modification (function):  molecular association, regulation, protein stabilization
 Effect of modification (process):  carcinogenesis, induced, cell growth, induced, transcription, induced
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
ER-alpha (human) Disrupts co-immunoprecipitation
DNA Disrupts in vitro
Associated Diseases
Diseases: Alterations: Comments:
breast cancer increased


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