Wu Y, et al. (2014) Phosphorylation of p53 by TAF1 inactivates p53-dependent transcription in the DNA damage response. Mol Cell 53, 63-74 24289924

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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T183-p - AMPKA1 (human) ▲

Modsite: sDGEFLRtsCGsPNy SwissProt Entrez-Gene Orthologous residues AMPKA1 (human): T183‑p, AMPKA1 iso2 (human): T198‑p, AMPKA1 (mouse): T183‑p, AMPKA1 (rat): T183‑p, AMPKA1 (fruit fly): T184‑p Characterization Methods used to characterize site in vivo:  phospho-antibody, western blotting Disease tissue studied:  bone cancer Relevant cell lines - cell types - tissues:  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 UV increase 4-AN UV inhibit treatment-induced increase compound_C UV inhibit treatment-induced increase

T55-p - p53 (human) ▲

Modsite: DDIEQWFtEDPGPDE SwissProt Entrez-Gene Orthologous residues p53 (human): T55‑p, p53 iso2 (human): T55‑p, p53 iso4 (human): T16‑p, p53 (mouse): E55‑p, p53 iso2 (mouse): E55‑p, p53 (rat): E57‑p, p53 (rabbit): N54‑p, p53 (green monkey): T55‑p Characterization Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting Disease tissue studied:  bone cancer Relevant cell lines - cell types - tissues:  U2OS (bone cell) Cellular systems studied:  cell lines Species studied:  human Enzymes shown to modify site in vitro:  Type Enzyme KINASE TAF1 (human) Upstream Regulation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes UV increase 4-AN UV inhibit treatment-induced increase compound_C UV inhibit treatment-induced increase Downstream Regulation Effect of modification (function):  molecular association, regulation Effect of modification (process):  transcription, inhibited Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays Disrupts transcription, inhibited pull-down assay, co-immunoprecipitation Comments:  p53 dissociation from promoter late in DNA damage response

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, mutation of modification site Disease tissue studied:  bone cancer Relevant cell lines - cell types - tissues:  U2OS (bone cell) Cellular systems studied:  cell lines Species studied:  human Downstream Regulation Comments:  acetylation is required for T55 phosphorylation

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 Disease tissue studied:  bone cancer Relevant cell lines - cell types - tissues:  U2OS (bone cell) Cellular systems studied:  cell lines Species studied:  human Downstream Regulation Comments:  acetylation is required for T55 phosphorylation