Curated Information
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PubMed Id: 18637808 
Knauer O, et al. (2008) Differential phosphoproteome profiling reveals a functional role for VASP in Helicobacter pylori-induced cytoskeleton turnover in gastric epithelial cells. Cell Microbiol 10, 2285-96 18637808
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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S157-p - VASP (human)
Orthologous residues
VASP (human): S157‑p, VASP (mouse): S153‑p, VASP (rat): S154‑p
Characterization
 Methods used to characterize site in vivo immunoprecipitation, mass spectrometry, mutation of modification site, western blotting
 Disease tissue studied:  gastric cancer, gastric carcinoma
 Relevant cell lines - cell types - tissues:  AGS (gastric), MKN-28 (gastric)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PKCA (human) pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
bacterial infection increase Helicobacter pylori infection
KT5823 bacterial infection no effect upon treatment-induced increase
rottlerin bacterial infection decrease
Downstream Regulation
 Effect of modification (process):  cytoskeletal reorganization
 Comments:  H. pylori-induced cell elongation

S239-p - VASP (human)
Orthologous residues
VASP (human): S239‑p, VASP (mouse): S235‑p, VASP (rat): S236‑p
Characterization
 Methods used to characterize site in vivo immunoprecipitation, mass spectrometry, mutation of modification site, western blotting
 Disease tissue studied:  gastric cancer, gastric carcinoma
 Relevant cell lines - cell types - tissues:  AGS (gastric), MKN-28 (gastric)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PKG1 (human) pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
bacterial infection increase Helicobacter pylori infection
KT5823 bacterial infection decrease
rottlerin bacterial infection no effect upon treatment-induced increase
Downstream Regulation
 Effect of modification (process):  cytoskeletal reorganization
 Comments:  H. pylori-induced cell elongation

T278-p - VASP (human)
Orthologous residues
VASP (human): T278‑p, VASP (mouse): T274‑p, VASP (rat): T274‑p
Characterization
 Methods used to characterize site in vivo immunoprecipitation, mass spectrometry, mutation of modification site, western blotting
 Disease tissue studied:  gastric cancer, gastric carcinoma
 Relevant cell lines - cell types - tissues:  AGS (gastric), MKN-28 (gastric)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PKG1 (human) pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
bacterial infection increase Helicobacter pylori infection
KT5823 bacterial infection decrease
rottlerin bacterial infection no effect upon treatment-induced increase
Downstream Regulation
 Effect of modification (process):  cytoskeletal reorganization
 Comments:  H. pylori-induced cell elongation


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