Curated Information
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Home > Curated Information Page > PubMed Id: 18485870
Tang Y, et al. (2008) Acetylation is indispensable for p53 activation. Cell 133, 612-26 18485870
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, 2015, 43:D512-20). To learn more about the scope of PhosphoSitePlus®, click here.
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K120-ac - p53 (human)
Modsite: FLhSGTAkSVTCTyS SwissProt Entrez-Gene
Orthologous residues
p53 (human): K120‑ac, p53 iso2 (human): K120‑ac, p53 iso4 (human): K81‑ac, p53 (mouse): K117‑ac, p53 iso2 (mouse): K117‑ac, p53 (rat): K118‑ac, p53 (rabbit): K117‑ac, p53 (green 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)
Modsite: VRAMAIYkQSQHMTE SwissProt Entrez-Gene
Orthologous residues
p53 (human): K164‑ac, p53 iso2 (human): K164‑ac, p53 iso4 (human): K125‑ac, p53 (mouse): K161‑ac, p53 iso2 (mouse): K161‑ac, p53 (rat): K162‑ac, p53 (rabbit): K161‑ac, p53 (green 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 CBP (human)
ACETYLTRANSFERASE p300 (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)
Modsite: RAHsSHLkskkGQst SwissProt Entrez-Gene
Orthologous residues
p53 (human): K370‑ac, p53 iso2 (human): , p53 iso4 (human): K331‑ac, p53 (mouse): K367‑ac, p53 iso2 (mouse): , p53 (rat): K368‑ac, p53 (rabbit): K368‑ac, p53 (green 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)
Modsite: HsSHLkskkGQstsR SwissProt Entrez-Gene
Orthologous residues
p53 (human): K372‑ac, p53 iso2 (human): , p53 iso4 (human): K333‑ac, p53 (mouse): K369‑ac, p53 iso2 (mouse): , p53 (rat): K370‑ac, p53 (rabbit): K370‑ac, p53 (green 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)
Modsite: sSHLkskkGQstsRH SwissProt Entrez-Gene
Orthologous residues
p53 (human): K373‑ac, p53 iso2 (human): , p53 iso4 (human): K334‑ac, p53 (mouse): K370‑ac, p53 iso2 (mouse): , p53 (rat): K371‑ac, p53 (rabbit): K371‑ac, p53 (green 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)
Modsite: GQstsRHkkLMFktE SwissProt Entrez-Gene
Orthologous residues
p53 (human): K381‑ac, p53 iso2 (human): , p53 iso4 (human): K342‑ac, p53 (mouse): K378‑ac, p53 iso2 (mouse): , p53 (rat): K379‑ac, p53 (rabbit): K379‑ac, p53 (green 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)
Modsite: QstsRHkkLMFktEG SwissProt Entrez-Gene
Orthologous residues
p53 (human): K382‑ac, p53 iso2 (human): , p53 iso4 (human): K343‑ac, p53 (mouse): K379‑ac, p53 iso2 (mouse): , p53 (rat): K380‑ac, p53 (rabbit): K380‑ac, p53 (green 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)
Modsite: RHkkLMFktEGPDsD SwissProt Entrez-Gene
Orthologous residues
p53 (human): K386‑ac, p53 iso2 (human): , p53 iso4 (human): K347‑ac, p53 (mouse): K383‑ac, p53 iso2 (mouse): , p53 (rat): K384‑ac, p53 (rabbit): K384‑ac, p53 (green 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;