Curated Information
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Curated Information Page
PubMed Id: 12110590 
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.
Ouwens DM, et al. (2002) Growth factors can activate ATF2 via a two-step mechanism: phosphorylation of Thr71 through the Ras-MEK-ERK pathway and of Thr69 through RalGDS-Src-p38. EMBO J 21, 3782-93 12110590
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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T69-p - ATF-2 (human) ▲
Orthologous residues
ATF‑2 (human): T69‑p, ATF‑2 (mouse): T51‑p, ATF‑2 (rat): T51‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  3T3 (fibroblast) [InsR (human)], fibroblast, MEF (fibroblast)
 Cellular systems studied:  cell lines, primary cells
 Species studied:  human, mouse
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE JNK1 (human) pharmacological activator of upstream enzyme, phospho-antibody, genetic knockout/knockin of upstream enzyme
KINASE p38-alpha (human) inhibition of upstream enzyme, pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody, activation of upstream enzyme
KINASE JNK2 (human) pharmacological activator of upstream enzyme, phospho-antibody, genetic knockout/knockin of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
serum increase
EGF increase
UV increase
Downstream Regulation
 Effect of modification (process):  transcription, altered

T71-p - ATF-2 (human) ▲
Orthologous residues
ATF‑2 (human): T71‑p, ATF‑2 (mouse): T53‑p, ATF‑2 (rat): T53‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  3T3 (fibroblast) [InsR (human)], fibroblast, MEF (fibroblast)
 Cellular systems studied:  cell lines, primary cells
 Species studied:  human, mouse
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE ERK2 (human)
KINASE ERK1 (human)
KINASE p38-alpha (mouse)
KINASE JNK1 (mouse)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE JNK1 (human) pharmacological activator of upstream enzyme, phospho-antibody, genetic knockout/knockin of upstream enzyme
KINASE p38-alpha (human) inhibition of upstream enzyme, pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody, activation of upstream enzyme
KINASE JNK2 (human) pharmacological activator of upstream enzyme, phospho-antibody, genetic knockout/knockin of upstream enzyme
KINASE ERK1 (human) inhibition of upstream enzyme, pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody
KINASE ERK2 (human) inhibition of upstream enzyme, pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
serum increase
EGF increase
UV increase
Downstream Regulation
 Effect of modification (process):  transcription, altered

T51-p - ATF-2 (mouse) ▲
Orthologous residues
ATF‑2 (human): T69‑p, ATF‑2 (mouse): T51‑p, ATF‑2 (rat): T51‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  3T3 (fibroblast) [InsR (human)], fibroblast, MEF (fibroblast)
 Cellular systems studied:  cell lines, primary cells
 Species studied:  human, mouse
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE JNK1 (human) pharmacological activator of upstream enzyme, phospho-antibody, genetic knockout/knockin of upstream enzyme
KINASE p38-alpha (human) inhibition of upstream enzyme, pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody, activation of upstream enzyme
KINASE JNK2 (human) pharmacological activator of upstream enzyme, phospho-antibody, genetic knockout/knockin of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
insulin increase
insulin HRas (human) inhibit treatment-induced increase dominant negative
EGF increase
osmotic stress increase
osmotic stress HRas (human) no effect upon treatment-induced increase dominant negative
phorbol ester no change compared to control
EGF JNK1 (mouse), JNK2 (mouse) increase homozygous null
SB203580 EGF JNK1 (mouse), JNK2 (mouse) inhibit treatment-induced increase
PP1 EGF JNK1 (mouse), JNK2 (mouse) inhibit treatment-induced increase
serum JNK1 (mouse), JNK2 (mouse) increase homozygous null
SB203580 serum JNK1 (mouse), JNK2 (mouse) inhibit treatment-induced increase
PP1 serum JNK1 (mouse), JNK2 (mouse) inhibit treatment-induced increase
RalA (human) increase constitutively active
RLF (human) increase activated

T53-p - ATF-2 (mouse) ▲
Orthologous residues
ATF‑2 (human): T71‑p, ATF‑2 (mouse): T53‑p, ATF‑2 (rat): T53‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  3T3 (fibroblast) [InsR (human)], fibroblast, MEF (fibroblast)
 Cellular systems studied:  cell lines, primary cells
 Species studied:  human, mouse
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ERK2 (human) inhibition of upstream enzyme, pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody
KINASE ERK1 (human) inhibition of upstream enzyme, pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody
KINASE JNK2 (human) pharmacological activator of upstream enzyme, phospho-antibody, genetic knockout/knockin of upstream enzyme
KINASE JNK1 (human) pharmacological activator of upstream enzyme, phospho-antibody, genetic knockout/knockin of upstream enzyme
KINASE p38-alpha (human) inhibition of upstream enzyme, pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody, activation of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
insulin increase
insulin HRas (human) inhibit treatment-induced increase dominant negative
insulin RalA (human) no effect upon treatment-induced increase dominant negative
EGF increase
osmotic stress increase
osmotic stress HRas (human) no effect upon treatment-induced increase dominant negative
osmotic stress RalA (human) no effect upon treatment-induced increase dominant negative
phorbol ester increase
U0126 phorbol ester inhibit treatment-induced increase
EGF JNK1 (mouse), JNK2 (mouse) increase homozygous null
SB203580 EGF JNK1 (mouse), JNK2 (mouse) no effect upon treatment-induced increase slight decrease
U0126 EGF JNK1 (mouse), JNK2 (mouse) inhibit treatment-induced increase
SB203580 U0126 augment treatment-induced decrease
serum JNK1 (mouse), JNK2 (mouse) increase homozygous null
SB203580 serum JNK1 (mouse), JNK2 (mouse) no effect upon treatment-induced increase
PP1 serum JNK1 (mouse), JNK2 (mouse) inhibit treatment-induced increase
MMS JNK1 (mouse), JNK2 (mouse) increase homozygous null
SB203580 MMS JNK1 (mouse), JNK2 (mouse) inhibit treatment-induced increase
UV JNK1 (mouse), JNK2 (mouse) increase homozygous null
SB203580 UV JNK1 (mouse), JNK2 (mouse) inhibit treatment-induced increase
insulin JNK1 (mouse), JNK2 (mouse) increase homozygous null
SB203580 insulin JNK1 (mouse), JNK2 (mouse) inhibit treatment-induced increase
U0126 insulin JNK1 (mouse), JNK2 (mouse) inhibit treatment-induced increase
SB203580 U0126 augment treatment-induced decrease
RalA (human) increase constitutively active
RLF (human) increase activated


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