Curated Information
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Curated Information Page
PubMed Id: 15782121 
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.
Zhang R, et al. (2005) Hsp90-Akt phosphorylates ASK1 and inhibits ASK1-mediated apoptosis. Oncogene 24, 3954-63 15782121
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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S83-p - ASK1 (human) ▲
Orthologous residues
ASK1 (human): S83‑p, ASK1 iso5 (human): S163‑p, ASK1 (mouse): S90‑p, ASK1 (rat): S54‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  BAEC (endothelial), MEF (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  cow, mouse
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Akt1 (human) genetic knockout/knockin of upstream enzyme, phospho-antibody, co-immunoprecipitation, pharmacological activator of upstream enzyme, activation of upstream enzyme, pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
H2O2 decrease
H2O2 HSP90A (human) inhibit treatment-induced decrease
LY294002 decrease
17-AAG decrease
Downstream Regulation
 Effect of modification (function):  phosphorylation
 Effect of modification (process):  transcription, altered
 Comments:  phosphorylation of Ask1 T838

T838-p - ASK1 (human) ▲
Orthologous residues
ASK1 (human): T838‑p, ASK1 iso5 (human): T918‑p, ASK1 (mouse): T845‑p, ASK1 (rat): T809‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  BAEC (endothelial), MEF (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  cow, mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
H2O2 increase
H2O2 HSP90A (human) inhibit treatment-induced increase
LY294002 H2O2 augment treatment-induced increase
17-AAG H2O2 augment treatment-induced increase
LY294002 increase
17-AAG LY294002 augment treatment-induced increase

T180-p - p38-alpha (human) ▲
Orthologous residues
p38‑alpha (human): T180‑p, p38‑alpha iso2 (human): T180‑p, p38‑alpha (mouse): T180‑p, p38‑alpha (rat): T180‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  BAEC (endothelial), MEF (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  cow, mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
H2O2 increase
LY294002 H2O2 augment treatment-induced increase
17-AAG H2O2 augment treatment-induced increase

Y182-p - p38-alpha (human) ▲
Orthologous residues
p38‑alpha (human): Y182‑p, p38‑alpha iso2 (human): Y182‑p, p38‑alpha (mouse): Y182‑p, p38‑alpha (rat): Y182‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  BAEC (endothelial), MEF (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  cow, mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
H2O2 increase
LY294002 H2O2 augment treatment-induced increase
17-AAG H2O2 augment treatment-induced increase

S90-p - ASK1 (mouse) ▲
Orthologous residues
ASK1 (human): S83‑p, ASK1 iso5 (human): S163‑p, ASK1 (mouse): S90‑p, ASK1 (rat): S54‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  BAEC (endothelial), MEF (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  cow, mouse
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Akt1 (human) genetic knockout/knockin of upstream enzyme, phospho-antibody, co-immunoprecipitation, pharmacological activator of upstream enzyme, activation of upstream enzyme, pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
H2O2 decrease
Akt1 (mouse) decrease homozygous null

T845-p - ASK1 (mouse) ▲
Orthologous residues
ASK1 (human): T838‑p, ASK1 iso5 (human): T918‑p, ASK1 (mouse): T845‑p, ASK1 (rat): T809‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  BAEC (endothelial), MEF (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  cow, mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
H2O2 increase
H2O2 HSP90A (human) inhibit treatment-induced increase
Akt1 (mouse) increase homozygous null

T180-p - p38-alpha (mouse) ▲
Orthologous residues
p38‑alpha (human): T180‑p, p38‑alpha iso2 (human): T180‑p, p38‑alpha (mouse): T180‑p, p38‑alpha (rat): T180‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  BAEC (endothelial), MEF (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  cow, mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
H2O2 increase
H2O2 HSP90A (human) inhibit treatment-induced increase
H2O2 Akt1 (mouse) augment treatment-induced increase homozygous null
HSP90A (human) Akt1 (mouse) no effect upon treatment-induced increase
Akt1 (mouse) increase homozygous null

Y182-p - p38-alpha (mouse) ▲
Orthologous residues
p38‑alpha (human): Y182‑p, p38‑alpha iso2 (human): Y182‑p, p38‑alpha (mouse): Y182‑p, p38‑alpha (rat): Y182‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  BAEC (endothelial), MEF (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  cow, mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
H2O2 increase
H2O2 HSP90A (human) inhibit treatment-induced increase
H2O2 Akt1 (mouse) augment treatment-induced increase homozygous null
HSP90A (human) Akt1 (mouse) no effect upon treatment-induced increase
Akt1 (mouse) increase homozygous null

S473-p - Akt1 (cow) ▲
Orthologous residues
Akt1 (human): S473‑p, Akt1 (mouse): S473‑p, Akt1 (rat): S473‑p, Akt1 (fruit fly): S586‑p, Akt1 (cow): S473‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  BAEC (endothelial), MEF (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  cow, mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
H2O2 decrease
H2O2 HSP90A (human) inhibit treatment-induced decrease


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