Curated Information
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Curated Information Page
PubMed Id: 19573808 
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.
Miao H, et al. (2009) EphA2 mediates ligand-dependent inhibition and ligand-independent promotion of cell migration and invasion via a reciprocal regulatory loop with Akt. Cancer Cell 16, 9-20 19573808
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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T308-p - Akt1 (human)
Orthologous residues
Akt1 (human): T308‑p, Akt1 (mouse): T308‑p, Akt1 (rat): T308‑p, Akt1 (fruit fly): T423‑p, Akt1 (cow): T308‑p
Characterization
 Methods used to characterize site in vivo phospho-antibody, western blotting
 Disease tissue studied:  brain cancer, glioblastoma multiforme, glioma
 Relevant cell lines - cell types - tissues:  293 (epithelial), U373 MG (glial)
 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
serum increase
ephrin A1 serum inhibit treatment-induced increase

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:  brain cancer, glioblastoma multiforme, glioma
 Relevant cell lines - cell types - tissues:  293 (epithelial), U373 MG (glial)
 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
serum increase
ephrin A1 serum inhibit treatment-induced increase
serum increase
LY294002 serum inhibit treatment-induced increase

S897-p - EphA2 (human)
Orthologous residues
EphA2 (human): S897‑p, EphA2 (mouse): S898‑p, EphA2 (rat): S898‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  brain cancer, glioblastoma multiforme, glioma
 Relevant cell lines - cell types - tissues:  293 (epithelial), U373 MG (glial)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Akt1 (human) mutation in upstream enzyme recognition motif, activation of upstream enzyme, modification site within consensus motif
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
serum increase Serum + Fc
ephrin A1 serum inhibit treatment-induced increase Ephrin A1-Fc
SU5402 serum no effect upon treatment-induced increase
serum no effect upon treatment-induced increase 1-(2-Amino-6-(3,5-dimethoxyphenyl)pyrido[2,3-d]pyr- imidin-7-yl)-3-tert-butyl urea slight inhibition
EGF increase EGF + Fc
ephrin A1 EGF inhibit treatment-induced increase Ephrin A1-Fc
FGF2 increase + Fc
ephrin A1 FGF2 inhibit treatment-induced increase Ephrin A1-Fc
SU5402 FGF2 inhibit treatment-induced increase
FGF2 inhibit treatment-induced increase 1-(2-Amino-6-(3,5-dimethoxyphenyl)pyrido[2,3-d]pyr- imidin-7-yl)-3-tert-butyl urea (BU)
PDGF increase PDGF + Fc
LPA no change compared to control + Fc
ephrin A1 LPA no change compared to control Ephrin A1-Fc
Downstream Regulation
 Effect of modification (function):  intracellular localization
 Effect of modification (process):  carcinogenesis, induced, cell motility, altered
 Comments:  regulates cell migration and invasion; required for leading edge localization and cell polarization; high levels in grade IV astrocytomas (GBM samples)
Associated Diseases
Diseases: Alterations: Comments:
glioblastoma multiforme increased high levels in grade IV astrocytomas (GBM)


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