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Home > Curated Information Page > PubMed Id: 21930785
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.
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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