Curated Information
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Curated Information Page
PubMed Id: 20952396 
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.
Simboeck E, et al. (2010) A phosphorylation switch regulates the transcriptional activation of cell cycle regulator p21 by histone deacetylase inhibitors. J Biol Chem 285, 41062-73 20952396
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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S11-p - H3 (human) ▲
Orthologous residues
H3 (human): S11‑p, H3 (mouse): S11‑p, H3 iso2 (mouse): S11‑p, H3 iso3 (mouse): S11‑p, H3 (rat): S11‑p, H3 iso3 (rat): S11‑p, H3 (pig): S11‑p, H3 (chicken): S11‑p, H3 (cow): S11‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, modification-specific antibody
 Disease tissue studied:  brain cancer, glioblastoma multiforme, glioma
 Relevant cell lines - cell types - tissues:  T98G (glial)
 Cellular systems studied:  cell lines
 Species studied:  human
 Comments:  ChIP assay
 Enzymes shown to modify site in vitro: 
Type Enzyme
PHOSPHATASE PPP2CA (mouse)
 Comments:  inhibited by 14-3-3 zeta
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
anisomycin, trichostatin A increase
anisomycin, trichostatin A MSK1 (human) increase MSK1 siRNA inhibits

K15-a - H3 (human) ▲
Orthologous residues
H3 (human): K15‑a, H3 (mouse): K15‑a, H3 iso2 (mouse): K15‑a, H3 iso3 (mouse): K15‑a, H3 (rat): K15‑a, H3 iso3 (rat): K15‑a, H3 (pig): K15‑a, H3 (chicken): K15‑a, H3 (cow): K15‑a
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, modification-specific antibody
 Disease tissue studied:  brain cancer, glioblastoma multiforme, glioma
 Relevant cell lines - cell types - tissues:  T98G (glial)
 Cellular systems studied:  cell lines
 Species studied:  human
 Comments:  ChIP assay
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
anisomycin, trichostatin A increase
anisomycin, trichostatin A MSK1 (human) increase MSK1 siRNA inhibits

S11-p - H3 (mouse) ▲
Orthologous residues
H3 (human): S11‑p, H3 (mouse): S11‑p, H3 iso2 (mouse): S11‑p, H3 iso3 (mouse): S11‑p, H3 (rat): S11‑p, H3 iso3 (rat): S11‑p, H3 (pig): S11‑p, H3 (chicken): S11‑p, H3 (cow): S11‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, modification-specific antibody
 Relevant cell lines - cell types - tissues:  3T3 (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  mouse
 Comments:  ChIP assay
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
anisomycin, trichostatin A increase
H-89 anisomycin, trichostatin A inhibit treatment-induced increase
anisomycin, trichostatin A increase
trichostatin A increase
okadaic acid increase
okadaic acid trichostatin A augment treatment-induced increase
anisomycin, trichostatin A 14-3-3 zeta (mouse) inhibit treatment-induced increase

K15-a - H3 (mouse) ▲
Orthologous residues
H3 (human): K15‑a, H3 (mouse): K15‑a, H3 iso2 (mouse): K15‑a, H3 iso3 (mouse): K15‑a, H3 (rat): K15‑a, H3 iso3 (rat): K15‑a, H3 (pig): K15‑a, H3 (chicken): K15‑a, H3 (cow): K15‑a
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, modification-specific antibody
 Relevant cell lines - cell types - tissues:  3T3 (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  mouse
 Comments:  ChIP assay
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
anisomycin, trichostatin A increase
H-89 anisomycin, trichostatin A inhibit treatment-induced increase
anisomycin, trichostatin A increase
trichostatin A increase
okadaic acid increase
okadaic acid trichostatin A augment treatment-induced increase
anisomycin, trichostatin A 14-3-3 zeta (mouse) inhibit treatment-induced increase

S1619-p - POLR2A (mouse) ▲
Orthologous residues
POLR2A (human): S1619‑p, POLR2A var1 (human): S1619‑p, POLR2A (mouse): S1619‑p, POLR2A (rat): S1619‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, modification-specific antibody
 Relevant cell lines - cell types - tissues:  3T3 (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  mouse
 Comments:  ChIP assay
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
anisomycin, trichostatin A increase
H-89 anisomycin, trichostatin A inhibit treatment-induced increase


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