Curated Information
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Curated Information Page
PubMed Id: 12151396 
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.
Maekawa M, Nishida E, Tanoue T (2002) Identification of the Anti-proliferative protein Tob as a MAPK substrate. J Biol Chem 277, 37783-7 12151396
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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S152-p - TOB1 (human) ▲
Orthologous residues
TOB1 (human): S152‑p, TOB1 (mouse): S152‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site
 Relevant cell lines - cell types - tissues:  3T3 (fibroblast) [SHP-2 (mouse), homozygous knockout]
 Cellular systems studied:  cell lines
 Species studied:  mouse
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE JNK2 (human)
KINASE ERK2 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ERK2 (human) co-immunoprecipitation, pharmacological inhibitor of upstream enzyme, pharmacological activator of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
aFGF increase
U0126 aFGF inhibit treatment-induced increase
EGF increase
U0126 EGF inhibit treatment-induced increase
serum increase
U0126 serum inhibit treatment-induced increase
PDGF increase
estrogen increase
Downstream Regulation
 Effect of modification (function):  inhibition
 Effect of modification (process):  cell cycle regulation
 Comments:  the antiproliferative function of TOB1 is inhibited by phosphorylation.

S154-p - TOB1 (human) ▲
Orthologous residues
TOB1 (human): S154‑p, TOB1 (mouse): S154‑p
Characterization
 Methods used to characterize site in vivo:  electrophoretic mobility shift, mutation of modification site
 Relevant cell lines - cell types - tissues:  3T3 (fibroblast) [SHP-2 (mouse), homozygous knockout], C2C12 (myoblast), COS (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  monkey, mouse
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE JNK2 (human)
KINASE ERK2 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ERK2 (human) co-immunoprecipitation, pharmacological inhibitor of upstream enzyme, pharmacological activator of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
aFGF increase
U0126 aFGF inhibit treatment-induced increase
EGF increase
U0126 EGF inhibit treatment-induced increase
serum increase
U0126 serum inhibit treatment-induced increase
PDGF increase
estrogen increase
Downstream Regulation
 Effect of modification (function):  inhibition
 Effect of modification (process):  cell cycle regulation
 Comments:  the antiproliferative function of TOB1 is inhibited by phosphorylation.

S164-p - TOB1 (human) ▲
Orthologous residues
TOB1 (human): S164‑p, TOB1 (mouse): S164‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site
 Relevant cell lines - cell types - tissues:  3T3 (fibroblast) [SHP-2 (mouse), homozygous knockout]
 Cellular systems studied:  cell lines
 Species studied:  mouse
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE JNK2 (human)
KINASE ERK2 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ERK2 (human) co-immunoprecipitation, pharmacological inhibitor of upstream enzyme, pharmacological activator of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
aFGF increase
U0126 aFGF inhibit treatment-induced increase
EGF increase
U0126 EGF inhibit treatment-induced increase
serum increase
U0126 serum inhibit treatment-induced increase
PDGF increase
estrogen increase
Downstream Regulation
 Effect of modification (function):  inhibition
 Effect of modification (process):  cell cycle regulation
 Comments:  the antiproliferative function of TOB1 is inhibited by phosphorylation.


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