Curated Information
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Curated Information Page
PubMed Id: 23899556 
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.
Montero JC, Seoane S, Pandiella A (2013) Phosphorylation of P-Rex1 at serine 1169 participates in IGF-1R signaling in breast cancer cells. Cell Signal 25, 2281-9 23899556
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 mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  breast cancer
 Relevant cell lines - cell types - tissues:  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 increase
KU-0063794 IGF-1 inhibit treatment-induced increase
BEZ235 IGF-1 inhibit treatment-induced increase

S1169-p - PREX1 (human)
Orthologous residues
PREX1 (human): S1169‑p, PREX1 (mouse): S1160‑p
Characterization
 Methods used to characterize site in vivo immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  breast cancer
 Relevant cell lines - cell types - tissues:  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
neuregulin increase
IGF-1 increase
FGF1 increase
KU-0063794 IGF-1 no effect upon treatment-induced increase
BEZ235 IGF-1 no effect upon treatment-induced increase
mTOR (human) increase mTOR shRNA inhibits
Downstream Regulation
 Effect of modification (process):  cell growth, induced
 Comments:  increased Rac activity

S240-p - S6 (human)
Orthologous residues
S6 (human): S240‑p, S6 (mouse): S240‑p, S6 (rat): S240‑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:  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 increase
KU-0063794 IGF-1 inhibit treatment-induced increase
BEZ235 IGF-1 inhibit treatment-induced increase

S244-p - S6 (human)
Orthologous residues
S6 (human): S244‑p, S6 (mouse): S244‑p, S6 (rat): S244‑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:  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 increase
KU-0063794 IGF-1 inhibit treatment-induced increase
BEZ235 IGF-1 inhibit treatment-induced increase


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