Curated Information
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Curated Information Page
PubMed Id: 20101208 
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.
Barone I, et al. (2010) Phosphorylation of the mutant K303R estrogen receptor alpha at serine 305 affects aromatase inhibitor sensitivity. Oncogene 29, 2404-14 20101208
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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S473-p - Akt1 (human)
Orthologous residues
Akt1 (human): S473‑p, Akt1 (mouse): S473‑p, Akt1 (rat): S473‑p, Akt1 (fruit fly): S586‑p, Akt1 (cow): S473‑p
Characterization
 Methods used to characterize site in vivo phospho-antibody, western blotting
 Disease tissue studied:  breast cancer
 Relevant cell lines - cell types - tissues:  CHO (fibroblast), MCF-7 (breast cell)
 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
IGF-1 ER-alpha (human) increase increase augmented in cells expressing K303R mutant ER-alpha
androsterone ER-alpha (human) increase in ER-alpha K303R mutant cells, elevated basal phosphorylation and no androsterone increase
anastrazole androsterone ER-alpha (human) inhibit treatment-induced increase
peptide inhibitor no change compared to control ER-alpha S305 peptide
peptide inhibitor IGF-1 ER-alpha (human) augment treatment-induced increase ER-alpha S305 peptide

S305-p - ER-alpha (human)
Orthologous residues
ER‑alpha (human): S305‑p, ER‑alpha (mouse): S309‑p, ER‑alpha (rat): S310‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site
 Disease tissue studied:  breast cancer
 Relevant cell lines - cell types - tissues:  MCF-7 (breast cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE Akt1 (human)
 Comments:  K303R mutation increases S305 phosphorylation
Downstream Regulation
 Effect of modification (function):  activity, induced
 Effect of modification (process):  cell growth, altered
 Comments:  in K303R mutant

Y1161-p - IGF1R (human)
Orthologous residues
IGF1R (human): Y1161‑p, IGF1R (mouse): Y1163‑p, IGF1R (rat): Y1162‑p, IGF1R (pig): Y1161‑p
Characterization
 Methods used to characterize site in vivo phospho-antibody, western blotting
 Disease tissue studied:  breast cancer
 Relevant cell lines - cell types - tissues:  CHO (fibroblast), MCF-7 (breast cell)
 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
IGF-1 ER-alpha (human) increase increase augmented in cells expressing K303R mutant ER-alpha
androsterone ER-alpha (human) increase in ER-alpha K303R mutant cells, elevated basal phosphorylation and no androsterone increase
anastrazole androsterone ER-alpha (human) inhibit treatment-induced increase
peptide inhibitor no change compared to control ER-alpha S305 peptide
peptide inhibitor IGF-1 ER-alpha (human) augment treatment-induced increase ER-alpha S305 peptide

Y612-p - IRS1 (human)
Orthologous residues
IRS1 (human): Y612‑p, IRS1 (mouse): Y608‑p, IRS1 (rat): Y608‑p
Characterization
 Methods used to characterize site in vivo phospho-antibody, western blotting
 Disease tissue studied:  breast cancer
 Relevant cell lines - cell types - tissues:  CHO (fibroblast), MCF-7 (breast cell)
 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
IGF-1 ER-alpha (human) increase increase augmented in cells expressing K303R mutant ER-alpha
androsterone ER-alpha (human) increase in ER-alpha K303R mutant cells, elevated basal phosphorylation and no androsterone increase
anastrazole androsterone ER-alpha (human) inhibit treatment-induced increase
peptide inhibitor no change compared to control ER-alpha S305 peptide
peptide inhibitor IGF-1 ER-alpha (human) augment treatment-induced increase ER-alpha S305 peptide


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