Curated Information
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Curated Information Page
PubMed Id: 18332134 
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.
Ha CH, et al. (2008) Protein kinase D-dependent phosphorylation and nuclear export of histone deacetylase 5 mediates vascular endothelial growth factor-induced gene expression and angiogenesis. J Biol Chem 283, 14590-9 18332134
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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S259-p - HDAC5 (human) ▲
Orthologous residues
HDAC5 (human): S259‑p, HDAC5 (mouse): S250‑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)
 Cellular systems studied:  cell lines
 Species studied:  cow
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PKD1 (human) activation of upstream enzyme, transfection of wild-type enzyme, phospho-antibody, siRNA inhibition of enzyme, transfection of inactive enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
VEGF increase
U73122 VEGF inhibit treatment-induced decrease
LY294002 VEGF no effect upon treatment-induced increase
GF109203X VEGF inhibit treatment-induced increase
Ro31-8425 VEGF inhibit treatment-induced increase
Go 6976 VEGF inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (function):  intracellular localization
 Effect of modification (process):  cell motility, altered, transcription, altered
 Comments:  required for VEGF-induced nuclear export, transcription of MEF2 and in vitro angiogenesis

S498-p - HDAC5 (human) ▲
Orthologous residues
HDAC5 (human): S498‑p, HDAC5 (mouse): S488‑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)
 Cellular systems studied:  cell lines
 Species studied:  cow
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PKD1 (human) activation of upstream enzyme, transfection of wild-type enzyme, phospho-antibody, siRNA inhibition of enzyme, transfection of inactive enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
VEGF increase
U73122 VEGF inhibit treatment-induced decrease
LY294002 VEGF no effect upon treatment-induced increase
GF109203X VEGF inhibit treatment-induced increase
Ro31-8425 VEGF inhibit treatment-induced increase
Go 6976 VEGF inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (function):  intracellular localization
 Effect of modification (process):  cell motility, altered, transcription, altered
 Comments:  required for VEGF-induced nuclear export, transcription of MEF2 and in vitro angiogenesis


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