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Home > Curated Information Page > PubMed Id: 23871434
Choi DW, et al. (2013) WIP1, a homeostatic regulator of the DNA damage response, is targeted by HIPK2 for phosphorylation and degradation. Mol Cell 51, 374-85 23871434
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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T119-p - HIPK2 (human)
Modsite: HNLMRRStVsLLDTY SwissProt Entrez-Gene
Orthologous residues
HIPK2 (human): T119‑p, HIPK2 (mouse): T119‑p, HIPK2 (rat): T119‑p
Characterization
Methods used to characterize site in vivo [32P] ATP in vitro, immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  colorectal cancer, colorectal carcinoma, lung cancer, non-small cell lung cancer
Relevant cell lines - cell types - tissues:  HCT116 (intestinal), NCI-H1299 (pulmonary)
Cellular systems studied:  cell lines
Species studied:  human
Enzymes shown to modify site in vitro
Type Enzyme
KINASE AMPKA1 (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE AMPKA2 (human) phospho-antibody, co-immunoprecipitation, siRNA inhibition of enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
ionizing_radiation increase
ATM (human) increase
cycloheximide ionizing_radiation inhibit treatment-induced increase
siRNA decrease AMPKA2-siRNA inhibits
Downstream Regulation
Effect of modification (function):  enzymatic activity, induced, molecular association, regulation, phosphorylation, protein stabilization
Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
PPM1D (human) Disrupts protein stabilization, phosphorylation co-immunoprecipitation
Comments:  increase protein stabilization and reduce phosphorylation of WIP1

S121-p - HIPK2 (human)
Modsite: LMRRStVsLLDTYQK SwissProt Entrez-Gene
Orthologous residues
HIPK2 (human): S121‑p, HIPK2 (mouse): S121‑p, HIPK2 (rat): S121‑p
Characterization
Methods used to characterize site in vivo [32P] ATP in vitro, immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  colorectal cancer, colorectal carcinoma, lung cancer, non-small cell lung cancer
Relevant cell lines - cell types - tissues:  HCT116 (intestinal), NCI-H1299 (pulmonary)
Cellular systems studied:  cell lines
Species studied:  human
Enzymes shown to modify site in vitro
Type Enzyme
KINASE AMPKA1 (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE AMPKA2 (human) phospho-antibody, co-immunoprecipitation, siRNA inhibition of enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
ionizing_radiation increase
ATM (human) increase
cycloheximide ionizing_radiation inhibit treatment-induced increase
siRNA decrease AMPKA2-siRNA inhibits
Downstream Regulation
Effect of modification (function):  enzymatic activity, induced, molecular association, regulation, phosphorylation, protein stabilization
Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
PPM1D (human) Disrupts protein stabilization, phosphorylation co-immunoprecipitation
Comments:  increase protein stabilization and reduce phosphorylation of WIP1

T1114-p - HIPK2 (human)
Modsite: APAALGStGTVAHLV SwissProt Entrez-Gene
Orthologous residues
HIPK2 (human): T1114‑p, HIPK2 (mouse): T1112‑p, HIPK2 (rat): T1111‑p
Characterization
Methods used to characterize site in vivo [32P] ATP in vitro, immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  colorectal cancer, colorectal carcinoma, lung cancer, non-small cell lung cancer
Relevant cell lines - cell types - tissues:  HCT116 (intestinal), NCI-H1299 (pulmonary)
Cellular systems studied:  cell lines
Species studied:  human
Enzymes shown to modify site in vitro
Type Enzyme
KINASE AMPKA1 (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE AMPKA2 (human) phospho-antibody, co-immunoprecipitation, siRNA inhibition of enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
ionizing_radiation increase
ATM (human) increase
cycloheximide ionizing_radiation inhibit treatment-induced increase
siRNA decrease AMPKA2-siRNA inhibits
Downstream Regulation
Effect of modification (function):  enzymatic activity, induced, molecular association, regulation, phosphorylation, protein stabilization
Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
PPM1D (human) Disrupts protein stabilization, phosphorylation co-immunoprecipitation
Comments:  increase protein stabilization and reduce phosphorylation of WIP1

S54-p - PPM1D (human)
Modsite: QPLPPRPsPAALPGG SwissProt Entrez-Gene
Orthologous residues
PPM1D (human): S54‑p, PPM1D (mouse): , PPM1D (rat):
Characterization
Methods used to characterize site in vivo mass spectrometry (in vitro), mutation of modification site, western blotting
Disease tissue studied:  colorectal cancer, colorectal carcinoma
Relevant cell lines - cell types - tissues:  HCT116 (intestinal), HeLa (cervical)
Cellular systems studied:  cell lines
Species studied:  human
Enzymes shown to modify site in vitro
Type Enzyme
KINASE HIPK2 (human)

S85-p - PPM1D (human)
Modsite: PLPDAGAsPAPsRCC SwissProt Entrez-Gene
Orthologous residues
PPM1D (human): S85‑p, PPM1D (mouse): S78‑p, PPM1D (rat): S78‑p
Characterization
Methods used to characterize site in vivo immunoprecipitation, mass spectrometry, mass spectrometry (in vitro), mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  colorectal cancer, colorectal carcinoma, lung cancer, non-small cell lung cancer
Relevant cell lines - cell types - tissues:  293 (epithelial), HCT116 (intestinal), HeLa (cervical), NCI-H1299 (pulmonary)
Cellular systems studied:  cell lines
Species studied:  human
Enzymes shown to modify site in vitro
Type Enzyme
KINASE HIPK2 (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE HIPK2 (human) co-immunoprecipitation, genetic knockout/knockin of upstream enzyme, genetic transfer of constitutively active upstream enzyme, siRNA inhibition of enzyme, transfection of inactive enzyme, transfection of wild-type enzyme, pharmacological inhibitor of upstream enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
ionizing_radiation decrease
siRNA decrease HIPK2-siRNA inhibits
okadaic_acid increase
siRNA okadaic_acid inhibit treatment-induced increase HIPK2-siRNA inhibits
SP600125 okadaic_acid no effect upon treatment-induced increase
U0126 okadaic_acid no effect upon treatment-induced increase
SB203580 okadaic_acid no effect upon treatment-induced increase
Downstream Regulation
Effect of modification (function):  protein degradation, ubiquitination
Effect of modification (process):  DNA repair, induced, signaling pathway regulation
Comments:  protein stabilization takes place after IR treatment and ATM activation