Curated Information
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Home > Curated Information Page > PubMed Id: 17996705
Li AG, et al. (2007) An acetylation switch in p53 mediates holo-TFIID recruitment. Mol Cell 28, 408-21 17996705
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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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 immunoprecipitation, mutation of modification site, western blotting
Disease tissue studied:  bone cancer, lung cancer, non-small cell lung cancer
Relevant cell lines - cell types - tissues:  NCI-H1299 (pulmonary), Saos-2 (bone cell), U2OS (bone cell)
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

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 immunoprecipitation, mutation of modification site, western blotting
Disease tissue studied:  bone cancer, lung cancer, non-small cell lung cancer
Relevant cell lines - cell types - tissues:  NCI-H1299 (pulmonary), Saos-2 (bone cell), U2OS (bone cell)
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

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 immunoprecipitation, modification-specific antibody, mutation of modification site, western blotting
Disease tissue studied:  bone cancer, lung cancer, non-small cell lung cancer
Relevant cell lines - cell types - tissues:  NCI-H1299 (pulmonary), Saos-2 (bone cell), U2OS (bone cell)
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
UV increase
Downstream Regulation
Effect of modification (function):  molecular association, regulation
Effect of modification (process):  transcription, induced
Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
Induces electrophoretic visualization
TAF1 (human) Bromodomain Induces in vitro, pull-down assay
Comments:  enhances p53-TAF1 complex binding to the p21 promoter

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 immunoprecipitation, mutation of modification site, western blotting
Disease tissue studied:  bone cancer, lung cancer, non-small cell lung cancer
Relevant cell lines - cell types - tissues:  NCI-H1299 (pulmonary), Saos-2 (bone cell), U2OS (bone cell)
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

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 immunoprecipitation, mutation of modification site, western blotting
Disease tissue studied:  bone cancer, lung cancer, non-small cell lung cancer
Relevant cell lines - cell types - tissues:  NCI-H1299 (pulmonary), Saos-2 (bone cell), U2OS (bone cell)
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
UV increase
Downstream Regulation
Effect of modification (function):  molecular association, regulation
Effect of modification (process):  transcription, induced
Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
TAF1 (human) Bromodomain Induces in vitro, pull-down assay
Induces electrophoretic visualization
Comments:  enhances p53-TAF1 complex binding to the p21 promoter

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