Huang Y, et al. (2008) ATM kinase is a master switch for the Delta Np63 alpha phosphorylation/degradation in human head and neck squamous cell carcinoma cells upon DNA damage. Cell Cycle 7, 2846-55 18769144

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.

Click on the protein name to open the protein page, and on the RSD number to open the site page.

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S479-p - p63 (human) ▲

Modsite: MNKLPsVsQLINPQQ SwissProt Entrez-Gene Orthologous residues p63 (human): S479‑p, p63 iso2 (human): S385‑p, p63 (mouse): S479‑p, p63 (rat): S479‑p Characterization Methods used to characterize site in vivo:  mass spectrometry, mutation of modification site, phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  HaCaT (keratinocyte) Cellular systems studied:  cell lines Species studied:  human Comments:  HNSCC 029 cells Enzymes shown to modify site in vitro:  Type Enzyme KINASE ATM (human) Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE ATM (human) pharmacological inhibitor of upstream enzyme, phospho-motif antibody Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes cisplatin increase KU-55933 cisplatin inhibit treatment-induced increase Downstream Regulation Effect of modification (function):  protein degradation

T491-p - p63 (human) ▲

Modsite: PQQRNALtPTTIPDG SwissProt Entrez-Gene Orthologous residues p63 (human): T491‑p, p63 iso2 (human): T397‑p, p63 (mouse): T491‑p, p63 (rat): T491‑p Characterization Methods used to characterize site in vivo:  mass spectrometry, mutation of modification site, phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  HaCaT (keratinocyte) Cellular systems studied:  cell lines Species studied:  human Comments:  HNSCC 029 cells Enzymes shown to modify site in vitro:  Type Enzyme KINASE CDK2 (human) Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE CDK2 (human) pharmacological inhibitor of upstream enzyme, phospho-motif antibody Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes cisplatin increase seliciclib cisplatin inhibit treatment-induced increase Downstream Regulation Effect of modification (function):  protein degradation

S560-p - p63 (human) ▲

Modsite: LARLGCSsCLDYFTT SwissProt Entrez-Gene Orthologous residues p63 (human): S560‑p, p63 iso2 (human): S466‑p, p63 (mouse): S560‑p, p63 (rat): S560‑p Characterization Methods used to characterize site in vivo:  mass spectrometry, mutation of modification site, phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  HaCaT (keratinocyte) Cellular systems studied:  cell lines Species studied:  human Comments:  HNSCC 029 cells Enzymes shown to modify site in vitro:  Type Enzyme KINASE p70S6K (human) Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE p70S6K (human) pharmacological inhibitor of upstream enzyme, phospho-motif antibody Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes cisplatin increase rapamycin cisplatin inhibit treatment-induced increase Downstream Regulation Effect of modification (function):  protein degradation