Curated Information
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Curated Information Page
PubMed Id: 17435750 
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.
Regad T, et al. (2007) The neural progenitor-specifying activity of FoxG1 is antagonistically regulated by CKI and FGF. Nat Cell Biol 9, 531-40 17435750
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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S19-p - FOXG1 (human)
Orthologous residues
FOXG1 (human): S19‑p, FOXG1 (mouse): S19‑p, FOXG1 (rat): S19‑p
Characterization
 Methods used to characterize site in vivo electrophoretic mobility shift, mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  embryo, HeLa (cervical), neuron-'brain, cerebral cortex'
 Cellular systems studied:  cell lines, primary cells, tissue
 Species studied:  frog, human, mouse
 Comments:  OP27 cells
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE CK1A (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE CK1A (human) modification site within consensus motif, pharmacological inhibitor of upstream enzyme, transfection of wild-type enzyme, electrophoretic mobility shift, phospho-motif antibody
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
CKI-7 decrease
D4476 decrease
IC261 decrease
Downstream Regulation
 Effect of modification (function):  intracellular localization
 Effect of modification (process):  cell differentiation, altered

T279-p - FOXG1 (human)
Orthologous residues
FOXG1 (human): T279‑p, FOXG1 (mouse): T271‑p, FOXG1 (rat): T270‑p
Characterization
 Methods used to characterize site in vivo electrophoretic mobility shift, mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  embryo, HeLa (cervical), neuron-'brain, cerebral cortex'
 Cellular systems studied:  cell lines, primary cells, tissue
 Species studied:  frog, human, mouse
 Comments:  OP27 cells
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Akt1 (human) activation of upstream enzyme, modification site within consensus motif, pharmacological inhibitor of upstream enzyme, phospho-motif antibody
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
FGFR1 (human) increase activated
SU5402 decrease
LY294002 decrease
decrease Akt inhibitor VIII
Downstream Regulation
 Effect of modification (function):  intracellular localization


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