Curated Information
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Curated Information Page
PubMed Id: 10949026 
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.
Datta SR, et al. (2000) 14-3-3 proteins and survival kinases cooperate to inactivate BAD by BH3 domain phosphorylation. Mol Cell 6, 41-51 10949026
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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S112-p - BAD (mouse)
Orthologous residues
BAD (human): S75‑p, BAD (mouse): S112‑p, BAD (rat): S113‑p
Characterization
 Methods used to characterize site in vivo electrophoretic mobility shift, mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  CCL39 (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  hamster
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE PKACA (mouse)

S136-p - BAD (mouse)
Orthologous residues
BAD (human): S99‑p, BAD (mouse): S136‑p, BAD (rat): S137‑p
Characterization
 Methods used to characterize site in vivo electrophoretic mobility shift, mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  CCL39 (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  hamster
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE PKACA (mouse)
KINASE Akt1 (mouse)
 Comments:  Major phosphoacceptor site for Akt1.
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PKACA (mouse) transfection of constitutively active enzyme
KINASE Akt1 (mouse) transfection of constitutively active enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
IGF-1 increase
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Effect of modification (process):  apoptosis, altered
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
14-3-3 beta (mouse) Induces activity, induced co-immunoprecipitation

S155-p - BAD (mouse)
Orthologous residues
BAD (human): S118‑p, BAD (mouse): S155‑p, BAD (rat): S156‑p
Characterization
 Methods used to characterize site in vivo electrophoretic mobility shift, mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  CCL39 (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  hamster
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE Akt1 (mouse)
KINASE PKACA (mouse)
 Comments:  Major phosphoacceptor site for PKA. Minor phosphoacceptor site for Akt1.
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Akt1 (mouse) transfection of constitutively active enzyme
KINASE PKACA (mouse) transfection of constitutively active enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
IGF-1 increase
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Effect of modification (process):  apoptosis, altered
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
Bcl-xL (mouse) Disrupts


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