Chandrasekaran S, Tan TX, Hall JR, Cook JG (2011) Stress-stimulated mitogen-activated protein kinases control the stability and activity of the cdt1 DNA replication licensing factor. Mol Cell Biol 31, 4405-16 21930785

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.

Download

S391-p - CDT1 (human) ▲

Modsite: LRSAAPssPGsPrPA SwissProt Entrez-Gene Orthologous residues CDT1 (human): S391‑p, CDT1 (mouse): S403‑p Characterization Methods used to characterize site in vivo:  mutation of modification site Disease tissue studied:  colorectal cancer, colorectal carcinoma Relevant cell lines - cell types - tissues:  E.coli (bacterial), fibroblast, HCT116 (intestinal), HeLa (cervical) Cellular systems studied:  cell lines, primary cells Species studied:  bacteria, human Enzymes shown to modify site in vitro:  Type Enzyme KINASE P38A (human) Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE P38A (human) siRNA inhibition of enzyme, pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody, co-immunoprecipitation KINASE JNK1 (human) siRNA inhibition of enzyme, pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody, co-immunoprecipitation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes sorbitol increase UV sorbitol inhibit treatment-induced increase SB203580 decrease nocodazole increase Downstream Regulation Effect of modification (function):  activity, inhibited, molecular association, regulation, protein stabilization Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays RAMP (human) Disrupts in vitro

T402-p - CDT1 (human) ▲

Modsite: PrPALPAtPPAtPPA SwissProt Entrez-Gene Orthologous residues CDT1 (human): T402‑p, CDT1 (mouse): T414‑p Characterization Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting Disease tissue studied:  colorectal cancer, colorectal carcinoma Relevant cell lines - cell types - tissues:  E.coli (bacterial), fibroblast, HCT116 (intestinal), HeLa (cervical) Cellular systems studied:  cell lines, primary cells Species studied:  bacteria, human Enzymes shown to modify site in vitro:  Type Enzyme KINASE P38A (human) Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE P38A (human) siRNA inhibition of enzyme, pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody, co-immunoprecipitation KINASE JNK1 (human) siRNA inhibition of enzyme, pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody, co-immunoprecipitation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes nocodazole increase sorbitol increase UV sorbitol inhibit treatment-induced increase SB203580 decrease Downstream Regulation Effect of modification (function):  activity, inhibited, molecular association, regulation, protein stabilization Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays RAMP (human) Disrupts in vitro

T406-p - CDT1 (human) ▲

Modsite: LPAtPPAtPPAAsPs SwissProt Entrez-Gene Orthologous residues CDT1 (human): T406‑p, CDT1 (mouse): T418‑p Characterization Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting Disease tissue studied:  colorectal cancer, colorectal carcinoma Relevant cell lines - cell types - tissues:  E.coli (bacterial), fibroblast, HCT116 (intestinal), HeLa (cervical) Cellular systems studied:  cell lines, primary cells Species studied:  bacteria, human Enzymes shown to modify site in vitro:  Type Enzyme KINASE P38A (human) Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE P38A (human) siRNA inhibition of enzyme, pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody, co-immunoprecipitation KINASE JNK1 (human) siRNA inhibition of enzyme, pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody, co-immunoprecipitation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes nocodazole increase sorbitol increase UV sorbitol inhibit treatment-induced increase SB203580 decrease Downstream Regulation Effect of modification (function):  activity, inhibited, molecular association, regulation, protein stabilization Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays RAMP (human) Disrupts in vitro

S411-p - CDT1 (human) ▲

Modsite: PAtPPAAsPsALkGV SwissProt Entrez-Gene Orthologous residues CDT1 (human): S411‑p, CDT1 (mouse): S423‑p Characterization Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting Disease tissue studied:  colorectal cancer, colorectal carcinoma Relevant cell lines - cell types - tissues:  E.coli (bacterial), fibroblast, HCT116 (intestinal), HeLa (cervical) Cellular systems studied:  cell lines, primary cells Species studied:  bacteria, human Enzymes shown to modify site in vitro:  Type Enzyme KINASE P38A (human) Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE P38A (human) siRNA inhibition of enzyme, pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody, co-immunoprecipitation KINASE JNK1 (human) siRNA inhibition of enzyme, pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody, co-immunoprecipitation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes nocodazole increase sorbitol increase UV sorbitol inhibit treatment-induced increase SB203580 decrease Downstream Regulation Effect of modification (function):  activity, inhibited, molecular association, regulation, protein stabilization Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays RAMP (human) Disrupts in vitro

S491-p - CDT1 (human) ▲

Modsite: GSCCTIMsPGEMEKH SwissProt Entrez-Gene Orthologous residues CDT1 (human): S491‑p, CDT1 (mouse): S503‑p Characterization Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting Disease tissue studied:  colorectal cancer, colorectal carcinoma Relevant cell lines - cell types - tissues:  E.coli (bacterial), fibroblast, HCT116 (intestinal), HeLa (cervical) Cellular systems studied:  cell lines, primary cells Species studied:  bacteria, human Enzymes shown to modify site in vitro:  Type Enzyme KINASE P38A (human) Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE P38A (human) siRNA inhibition of enzyme, pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody, co-immunoprecipitation KINASE JNK1 (human) siRNA inhibition of enzyme, pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody, co-immunoprecipitation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes nocodazole increase sorbitol increase UV sorbitol inhibit treatment-induced increase SB203580 decrease Downstream Regulation Effect of modification (function):  activity, inhibited, molecular association, regulation, protein stabilization Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays RAMP (human) Disrupts in vitro