Curated Information
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Curated Information Page
PubMed Id: 18485870 
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.
Tang Y, et al. (2008) Acetylation is indispensable for p53 activation. Cell 133, 612-26 18485870
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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K120-ac - p53 (human)
Orthologous residues
p53 (human): K120‑ac, p53 (mouse): K114‑ac, p53 iso2 (mouse): K117‑ac, p53 (rat): K118‑ac, p53 (rabbit): K117‑ac, p53 (monkey): K120‑ac
Characterization
 Methods used to characterize site in vivo mass spectrometry, mutation of modification site
 Disease tissue studied:  colorectal cancer, colorectal carcinoma, lung cancer, non-small cell lung cancer
 Relevant cell lines - cell types - tissues:  HCT116 (intestinal), NCI-H1299 (pulmonary)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
trichostatin A increase
nicotinamide increase
Downstream Regulation
 Effect of modification (process):  apoptosis, induced, transcription, altered
 Comments:  p53 8KR mutation (K120/164/370/372/373/381/382/386R) impairs p53-dependent transcription; p53 8KR mutant can be still degraded by Mdm2;

K164-ac - p53 (human)
Orthologous residues
p53 (human): K164‑ac, p53 (mouse): K158‑ac, p53 iso2 (mouse): K161‑ac, p53 (rat): K162‑ac, p53 (rabbit): K161‑ac, p53 (monkey): K164‑ac
Characterization
 Methods used to characterize site in vivo mass spectrometry, mutation of modification site, phospho-antibody
 Disease tissue studied:  colorectal cancer, colorectal carcinoma, lung cancer, non-small cell lung cancer
 Relevant cell lines - cell types - tissues:  HCT116 (intestinal), NCI-H1299 (pulmonary)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
ACETYLTRANSFERASE p300 (human)
ACETYLTRANSFERASE CBP (human)
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
etoposide augment treatment-induced decrease
trichostatin A increase
nicotinamide increase
Downstream Regulation
 Effect of modification (process):  apoptosis, induced, transcription, altered
 Comments:  p53 8KR mutation (K120/164/370/372/373/381/382/386R) impairs p53-dependent transcription; p53 8KR mutant can be still degraded by Mdm2;

K370-ac - p53 (human)
Orthologous residues
p53 (human): K370‑ac, p53 (mouse): K364‑ac, p53 iso2 (mouse): , p53 (rat): K368‑ac, p53 (rabbit): K368‑ac, p53 (monkey): K370‑ac
Characterization
 Methods used to characterize site in vivo mass spectrometry, mutation of modification site
 Disease tissue studied:  colorectal cancer, colorectal carcinoma, lung cancer, non-small cell lung cancer
 Relevant cell lines - cell types - tissues:  HCT116 (intestinal), NCI-H1299 (pulmonary)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
trichostatin A increase
nicotinamide increase
Downstream Regulation
 Effect of modification (process):  apoptosis, induced, transcription, altered
 Comments:  p53 8KR mutation (K120/164/370/372/373/381/382/386R) impairs p53-dependent transcription; p53 8KR mutant can be still degraded by Mdm2;

K372-ac - p53 (human)
Orthologous residues
p53 (human): K372‑ac, p53 (mouse): K366‑ac, p53 iso2 (mouse): , p53 (rat): K370‑ac, p53 (rabbit): K370‑ac, p53 (monkey): K372‑ac
Characterization
 Methods used to characterize site in vivo mass spectrometry, mutation of modification site
 Disease tissue studied:  colorectal cancer, colorectal carcinoma, lung cancer, non-small cell lung cancer
 Relevant cell lines - cell types - tissues:  HCT116 (intestinal), NCI-H1299 (pulmonary)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
trichostatin A increase
nicotinamide increase
Downstream Regulation
 Effect of modification (process):  apoptosis, induced, transcription, altered
 Comments:  p53 8KR mutation (K120/164/370/372/373/381/382/386R) impairs p53-dependent transcription; p53 8KR mutant can be still degraded by Mdm2;

K373-ac - p53 (human)
Orthologous residues
p53 (human): K373‑ac, p53 (mouse): K367‑ac, p53 iso2 (mouse): , p53 (rat): K371‑ac, p53 (rabbit): K371‑ac, p53 (monkey): K373‑ac
Characterization
 Methods used to characterize site in vivo mass spectrometry, mutation of modification site
 Disease tissue studied:  colorectal cancer, colorectal carcinoma, lung cancer, non-small cell lung cancer
 Relevant cell lines - cell types - tissues:  HCT116 (intestinal), NCI-H1299 (pulmonary)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
trichostatin A increase
nicotinamide increase
Downstream Regulation
 Effect of modification (process):  apoptosis, induced, transcription, altered
 Comments:  p53 8KR mutation (K120/164/370/372/373/381/382/386R) impairs p53-dependent transcription; p53 8KR mutant can be still degraded by Mdm2;

K381-ac - p53 (human)
Orthologous residues
p53 (human): K381‑ac, p53 (mouse): K375‑ac, p53 iso2 (mouse): , p53 (rat): K379‑ac, p53 (rabbit): K379‑ac, p53 (monkey): K381‑ac
Characterization
 Methods used to characterize site in vivo mass spectrometry, mutation of modification site
 Disease tissue studied:  colorectal cancer, colorectal carcinoma, lung cancer, non-small cell lung cancer
 Relevant cell lines - cell types - tissues:  HCT116 (intestinal), NCI-H1299 (pulmonary)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
trichostatin A increase
nicotinamide increase
Downstream Regulation
 Effect of modification (process):  apoptosis, induced, transcription, altered
 Comments:  p53 8KR mutation (K120/164/370/372/373/381/382/386R) impairs p53-dependent transcription; p53 8KR mutant can be still degraded by Mdm2;

K382-ac - p53 (human)
Orthologous residues
p53 (human): K382‑ac, p53 (mouse): K376‑ac, p53 iso2 (mouse): , p53 (rat): K380‑ac, p53 (rabbit): K380‑ac, p53 (monkey): K382‑ac
Characterization
 Methods used to characterize site in vivo mass spectrometry, mutation of modification site
 Disease tissue studied:  colorectal cancer, colorectal carcinoma, lung cancer, non-small cell lung cancer
 Relevant cell lines - cell types - tissues:  HCT116 (intestinal), NCI-H1299 (pulmonary)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
trichostatin A increase
nicotinamide increase
Downstream Regulation
 Effect of modification (process):  apoptosis, induced, transcription, altered
 Comments:  p53 8KR mutation (K120/164/370/372/373/381/382/386R) impairs p53-dependent transcription; p53 8KR mutant can be still degraded by Mdm2;

K386-ac - p53 (human)
Orthologous residues
p53 (human): K386‑ac, p53 (mouse): K380‑ac, p53 iso2 (mouse): , p53 (rat): K384‑ac, p53 (rabbit): K384‑ac, p53 (monkey): K386‑ac
Characterization
 Methods used to characterize site in vivo mass spectrometry, mutation of modification site
 Disease tissue studied:  colorectal cancer, colorectal carcinoma, lung cancer, non-small cell lung cancer
 Relevant cell lines - cell types - tissues:  HCT116 (intestinal), NCI-H1299 (pulmonary)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
trichostatin A increase
nicotinamide increase
Downstream Regulation
 Effect of modification (process):  apoptosis, induced, transcription, altered
 Comments:  p53 8KR mutation (K120/164/370/372/373/381/382/386R) impairs p53-dependent transcription; p53 8KR mutant can be still degraded by Mdm2;


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