Curated Information
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Curated Information Page
PubMed Id: 11035810 
Fang X, et al. (2000) Phosphorylation and inactivation of glycogen synthase kinase 3 by protein kinase A. Proc Natl Acad Sci U S A 97, 11960-5 11035810
This page summarizes selected information from the record 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.
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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S21-p - GSK3A (human)
Orthologous residues
GSK3A (human): S21‑p, GSK3A (mouse): S21‑p, GSK3A (rat): S21‑p, GSK3A (cow): S21‑p
Characterization
 Methods used to characterize site in vivo phospho-antibody
 Relevant cell lines - cell types - tissues:  293 (epithelial), 3T3 (fibroblast) [SHP-2 (mouse), homozygous knockout], Rat1 (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse, rat
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE PKACA (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PKACA (human) pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
cAMP analog increase
forskolin increase
LPA increase
isoproterenol increase
IGF-1 increase
IGF-1, wortmannin inhibit treatment-induced increase
IGF-1, LY294002 inhibit treatment-induced increase
IGF-1, H-89 no effect upon treatment-induced increase
Downstream Regulation
 Effect of modification (function):  enzymatic activity, inhibited

S9-p - GSK3B (human)
Orthologous residues
GSK3B (human): S9‑p, GSK3B iso2 (human): S9‑p, GSK3B (mouse): S9‑p, GSK3B (rat): S9‑p, GSK3B (rabbit): S3‑p
Characterization
 Methods used to characterize site in vivo phospho-antibody
 Relevant cell lines - cell types - tissues:  293 (epithelial), 3T3 (fibroblast) [SHP-2 (mouse), homozygous knockout], Rat1 (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse, rat
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE PKACA (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PKACA (human) pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
cAMP analog increase
forskolin increase
LPA increase
isoproterenol increase
IGF-1 increase
IGF-1, wortmannin inhibit treatment-induced increase
IGF-1, LY294002 inhibit treatment-induced increase
IGF-1, H-89 no effect upon treatment-induced increase
Downstream Regulation
 Effect of modification (function):  enzymatic activity, inhibited

S9-p - GSK3B (mouse)
Orthologous residues
GSK3B (human): S9‑p, GSK3B iso2 (human): S9‑p, GSK3B (mouse): S9‑p, GSK3B (rat): S9‑p, GSK3B (rabbit): S3‑p
Characterization
 Methods used to characterize site in vivo phospho-antibody
 Relevant cell lines - cell types - tissues:  293 (epithelial), 3T3 (fibroblast) [SHP-2 (mouse), homozygous knockout], Rat1 (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse, rat
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE PKACA (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PKACA (human) pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
cAMP analog increase
forskolin increase
LPA increase
isoproterenol increase
IGF-1 increase
IGF-1, wortmannin inhibit treatment-induced increase
IGF-1, LY294002 inhibit treatment-induced increase
IGF-1, H-89 no effect upon treatment-induced increase
Downstream Regulation
 Effect of modification (function):  enzymatic activity, inhibited

S21-p - GSK3A (rat)
Orthologous residues
GSK3A (human): S21‑p, GSK3A (mouse): S21‑p, GSK3A (rat): S21‑p, GSK3A (cow): S21‑p
Characterization
 Methods used to characterize site in vivo phospho-antibody
 Relevant cell lines - cell types - tissues:  293 (epithelial), 3T3 (fibroblast) [SHP-2 (mouse), homozygous knockout], Rat1 (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse, rat
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE PKACA (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PKACA (human) pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
cAMP analog increase
forskolin increase
LPA increase
isoproterenol increase
IGF-1 increase
IGF-1, wortmannin inhibit treatment-induced increase
IGF-1, LY294002 inhibit treatment-induced increase
IGF-1, H-89 no effect upon treatment-induced increase
Downstream Regulation
 Effect of modification (function):  enzymatic activity, inhibited


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