Curated Information
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PubMed Id: 17888676 
Ran R, et al. (2007) A novel 165-kDa Golgin protein induced by brain ischemia and phosphorylated by Akt protects against apoptosis. Mol Cell Neurosci 36, 392-407 17888676
This page summarizes selected information from the record 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.
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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S174-p - GOLGA3 (mouse)
Orthologous residues
GOLGA3 (human): S174‑p, GOLGA3 (mouse): S174‑p, GOLGA3 (rat): S134‑p
Characterization
 Methods used to characterize site in vivo microscopy-colocalization with upstream kinase, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  adrenal cancer, pheochromocytoma
 Relevant cell lines - cell types - tissues:  HeLa (cervical), PC-12 (chromaffin)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Akt1 (human) microscopy-colocalization, modification site within consensus motif, mutation in upstream enzyme recognition motif, co-immunoprecipitation, transfection of constitutively active enzyme S345 is the major site phosphorylated by Akt.
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
serum increase
PDGF increase
LY294002 PDGF, serum inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (process):  apoptosis, altered
 Comments:  protected against Brefeldin-A-induced apoptosis, but not Fas-mediated apoptosis.
Associated Diseases
Diseases: Alterations: Comments:
ischemia increased

S385-p - GOLGA3 (mouse)
Orthologous residues
GOLGA3 (human): S389‑p, GOLGA3 (mouse): S385‑p, GOLGA3 (rat): S345‑p
Characterization
 Methods used to characterize site in vivo microscopy-colocalization with upstream kinase, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  adrenal cancer, pheochromocytoma
 Relevant cell lines - cell types - tissues:  HeLa (cervical), PC-12 (chromaffin)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Akt1 (human) microscopy-colocalization, modification site within consensus motif, mutation in upstream enzyme recognition motif, co-immunoprecipitation, transfection of constitutively active enzyme S345 is the major site phosphorylated by Akt.
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
serum increase
PDGF increase
LY294002 PDGF, serum inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (process):  apoptosis, altered
 Comments:  protected against Brefeldin-A-induced apoptosis, but not Fas-mediated apoptosis.
Associated Diseases
Diseases: Alterations: Comments:
ischemia increased


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