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Home > Curated Information Page > PubMed Id: 11099047
Luo J, et al. (2000) Deacetylation of p53 modulates its effect on cell growth and apoptosis. Nature 408, 377-81 11099047
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 modification-specific antibody, mutation of modification site, western blotting
Disease tissue studied:  lung cancer, non-small cell lung cancer
Relevant cell lines - cell types - tissues:  MEF (fibroblast), NCI-H1299 (pulmonary)
Cellular systems studied:  cell lines
Species studied:  human, mouse
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
ACETYLTRANSFERASE p300 (human) transfection of wild-type enzyme
DEACETYLASE HDAC1 (human) pharmacological inhibitor of upstream enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
trichostatin_A increase
Downstream Regulation
Effect of modification (process):  apoptosis, induced, cell growth, inhibited, transcription, induced

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 modification-specific antibody, mutation of modification site, western blotting
Disease tissue studied:  lung cancer, non-small cell lung cancer
Relevant cell lines - cell types - tissues:  MEF (fibroblast), NCI-H1299 (pulmonary)
Cellular systems studied:  cell lines
Species studied:  human, mouse
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
DEACETYLASE HDAC1 (human) pharmacological inhibitor of upstream enzyme
ACETYLTRANSFERASE p300 (human) transfection of wild-type enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
trichostatin_A increase
Downstream Regulation
Effect of modification (process):  apoptosis, induced, cell growth, inhibited, transcription, induced

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 modification-specific antibody, mutation of modification site, western blotting
Disease tissue studied:  lung cancer, non-small cell lung cancer
Relevant cell lines - cell types - tissues:  MEF (fibroblast), NCI-H1299 (pulmonary)
Cellular systems studied:  cell lines
Species studied:  human, mouse
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
ACETYLTRANSFERASE p300 (human) transfection of wild-type enzyme
DEACETYLASE HDAC1 (human) pharmacological inhibitor of upstream enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
trichostatin_A increase
Downstream Regulation
Effect of modification (process):  apoptosis, induced, cell growth, inhibited, transcription, induced

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 modification-specific antibody, mutation of modification site, western blotting
Disease tissue studied:  lung cancer, non-small cell lung cancer
Relevant cell lines - cell types - tissues:  MEF (fibroblast), NCI-H1299 (pulmonary)
Cellular systems studied:  cell lines
Species studied:  human, mouse
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
DEACETYLASE HDAC1 (human) pharmacological inhibitor of upstream enzyme
ACETYLTRANSFERASE p300 (human) transfection of wild-type enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
trichostatin_A increase
Downstream Regulation
Effect of modification (process):  apoptosis, induced, cell growth, inhibited, transcription, induced

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 modification-specific antibody, mutation of modification site, western blotting
Disease tissue studied:  lung cancer, non-small cell lung cancer
Relevant cell lines - cell types - tissues:  MEF (fibroblast), NCI-H1299 (pulmonary)
Cellular systems studied:  cell lines
Species studied:  human, mouse
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
DEACETYLASE HDAC1 (human) pharmacological inhibitor of upstream enzyme
ACETYLTRANSFERASE p300 (human) transfection of wild-type enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
trichostatin_A increase
Downstream Regulation
Effect of modification (process):  apoptosis, induced, cell growth, inhibited, transcription, induced