Curated Information
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Curated Information Page
PubMed Id: 21602891 
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.
Sriram G, et al. (2011) Phosphorylation of Crk on tyrosine 251 in the RT loop of the SH3C domain promotes Abl kinase transactivation. Oncogene 30, 4645-55 21602891
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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Y226-p - Abl (human)
Orthologous residues
Abl (human): Y226‑p, Abl iso2 (human): Y245‑p, Abl (mouse): Y226‑p, Abl iso2 (mouse): Y245‑p, Abl (rat): Y226‑p, Abl iso2 (rat): Y245‑p
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
EGF increase
imatinib EGF inhibit treatment-induced increase

Y221-p - Crk (human)
Orthologous residues
Crk (human): Y221‑p, Crk iso2 (human): , Crk (mouse): Y221‑p, Crk iso3 (mouse): , Crk (rat): Y221‑p, Crk (chicken): Y222‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  breast cancer, breast adenocarcinoma, breast cancer, triple negative
 Relevant cell lines - cell types - tissues:  293T (epithelial), MDA-MB468 (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) transfection of wild-type enzyme, phospho-antibody
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
EGF increase
imatinib EGF inhibit treatment-induced increase

Y251-p - Crk (human)
Orthologous residues
Crk (human): Y251‑p, Crk iso2 (human): , Crk (mouse): Y251‑p, Crk iso3 (mouse): , Crk (rat): Y251‑p, Crk (chicken): Y252‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  breast cancer, breast adenocarcinoma, breast cancer, triple negative
 Relevant cell lines - cell types - tissues:  293T (epithelial), MDA-MB468 (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) transfection of wild-type enzyme, phospho-antibody, competition with site-specific peptide
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
EGF increase
imatinib EGF inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (function):  enzymatic activity, induced, molecular association, regulation
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
Shc2 (human) SH2 Induces pull-down assay
Arg (human) SH2 Induces pull-down assay
SHIP-2 (human) SH2 Induces pull-down assay
STAP1 (human) SH2 Induces pull-down assay
Abi-1 (human) SH2 Induces enzymatic activity, induced pull-down assay
 Comments:  Crk activates Abl through phospho-Y251.


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