Curated Information
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PubMed Id: 17591920 
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.
Makagiansar IT, Williams S, Mustelin T, Stallcup WB (2007) Differential phosphorylation of NG2 proteoglycan by ERK and PKCalpha helps balance cell proliferation and migration. J Cell Biol 178, 155-65 17591920
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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T202-p - ERK1 (human) ▲
Orthologous residues
ERK1 (human): T202‑p, ERK1 (mouse): T203‑p, ERK1 (rat): T203‑p, ERK1 (hamster): T192‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, phospho-antibody, western blotting
 Disease tissue studied:  brain cancer, glioblastoma, glioma, melanoma skin cancer
 Relevant cell lines - cell types - tissues:  A375 (melanocyte), U251 (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
U0126 serum inhibit treatment-induced increase
PDGF increase
U0126 PDGF inhibit treatment-induced increase
MEK1 (human) increase

Y204-p - ERK1 (human) ▲
Orthologous residues
ERK1 (human): Y204‑p, ERK1 (mouse): Y205‑p, ERK1 (rat): Y205‑p, ERK1 (hamster): Y194‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, phospho-antibody, western blotting
 Disease tissue studied:  brain cancer, glioblastoma, glioma, melanoma skin cancer
 Relevant cell lines - cell types - tissues:  A375 (melanocyte), U251 (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
U0126 serum inhibit treatment-induced increase
PDGF increase
U0126 PDGF inhibit treatment-induced increase
MEK1 (human) increase

T185-p - ERK2 (human) ▲
Orthologous residues
ERK2 (human): T185‑p, ERK2 (mouse): T183‑p, ERK2 (rat): T183‑p, ERK2 (chicken): T193‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, phospho-antibody, western blotting
 Disease tissue studied:  brain cancer, glioblastoma, glioma, melanoma skin cancer
 Relevant cell lines - cell types - tissues:  A375 (melanocyte), U251 (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
U0126 serum inhibit treatment-induced increase
PDGF increase
U0126 PDGF inhibit treatment-induced increase
MEK1 (human) increase

Y187-p - ERK2 (human) ▲
Orthologous residues
ERK2 (human): Y187‑p, ERK2 (mouse): Y185‑p, ERK2 (rat): Y185‑p, ERK2 (chicken): Y195‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, phospho-antibody, western blotting
 Disease tissue studied:  brain cancer, glioblastoma, glioma, melanoma skin cancer
 Relevant cell lines - cell types - tissues:  A375 (melanocyte), U251 (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
U0126 serum inhibit treatment-induced increase
PDGF increase
U0126 PDGF inhibit treatment-induced increase
MEK1 (human) increase

T638-p - PKCA (human) ▲
Orthologous residues
PKCA (human): T638‑p, PKCA (mouse): T638‑p, PKCA (rat): T638‑p, PKCA (cow): T638‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, phospho-antibody, western blotting
 Disease tissue studied:  brain cancer, glioblastoma, glioma, melanoma skin cancer
 Relevant cell lines - cell types - tissues:  A375 (melanocyte), U251 (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
PDGF increase
Go 6976 PDGF inhibit treatment-induced increase

T2256-p - NG2 (rat) ▲
Orthologous residues
NG2 (human): T2252‑p, NG2 (mouse): T2257‑p, NG2 (rat): T2256‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, phospho-antibody, western blotting
 Disease tissue studied:  brain cancer, glioblastoma, glioma, melanoma skin cancer
 Relevant cell lines - cell types - tissues:  A375 (melanocyte), U251 (glial)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PKCA (human) pharmacological inhibitor of upstream enzyme, activation of upstream enzyme, mutation in upstream enzyme recognition motif
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
PDGF increase
Go 6976 PDGF inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (function):  intracellular localization
 Effect of modification (process):  cell motility, altered

T2265-p - NG2 (rat) ▲
Orthologous residues
NG2 (human): T2261‑p, NG2 (mouse): T2266‑p, NG2 (rat): T2265‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, phospho-antibody, western blotting
 Disease tissue studied:  brain cancer, glioblastoma, glioma, melanoma skin cancer
 Relevant cell lines - cell types - tissues:  A375 (melanocyte), U251 (glial)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE ERK2 (mouse)

T2314-p - NG2 (rat) ▲
Orthologous residues
NG2 (human): T2310‑p, NG2 (mouse): T2315‑p, NG2 (rat): T2314‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, phospho-antibody, western blotting
 Disease tissue studied:  brain cancer, glioblastoma, glioma, melanoma skin cancer
 Relevant cell lines - cell types - tissues:  A375 (melanocyte), U251 (glial)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE ERK2 (mouse)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ERK2 (human) co-immunoprecipitation, pharmacological inhibitor of upstream enzyme, activation of upstream enzyme, mutation in upstream enzyme recognition motif
KINASE ERK1 (human) co-immunoprecipitation, pharmacological inhibitor of upstream enzyme, activation of upstream enzyme, mutation in upstream enzyme recognition motif
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
PDGF increase
U0126 PDGF inhibit treatment-induced increase
MEK1 (human) increase
Downstream Regulation
 Effect of modification (function):  intracellular localization
 Effect of modification (process):  cell growth, altered


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