Curated Information
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Curated Information Page
PubMed Id: 16940182 
This page summarizes selected information from the article referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2012,40:D261-70). To learn more about the scope of PhosphoSitePlus®, click here.
Buscemi G, et al. (2006) DNA damage-induced cell cycle regulation and function of novel Chk2 phosphoresidues. Mol Cell Biol 26, 7832-45 16940182
Only sites from this record are displayed on this page. Click on the protein name to open the protein page, and on the RSD number to open the site page. For the complete dataset, click the download button, on the right.
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S19-p - Chk2 (human) ▲
Orthologous residues
Chk2 (human): S19‑p, Chk2 iso12 (human): S19‑p, Chk2 (mouse): S22‑p, Chk2 (rat): S21‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody
 Relevant cell lines - cell types - tissues:  AT52RM (lymphoblastoid), GM07078 (lymphoblastoid), HCT15 (intestinal), LBC-N
 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
ionizing radiation increase
4-NQO no change compared to control
hydroxyurea no change compared to control
Downstream Regulation
 Effect of modification (function):  enzymatic activity, induced, molecular association, regulation
 Effect of modification (process):  cell cycle regulation
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
Chk2 (human) Induces
 Comments:  S19A mutant shows impaired dimerization and does not promote Hdmx degradation

S33-p - Chk2 (human) ▲
Orthologous residues
Chk2 (human): S33‑p, Chk2 iso12 (human): S33‑p, Chk2 (mouse): S36‑p, Chk2 (rat): S35‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody
 Relevant cell lines - cell types - tissues:  AT52RM (lymphoblastoid), GM07078 (lymphoblastoid), HCT15 (intestinal), LBC-N
 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
ionizing radiation increase
4-NQO no change compared to control
hydroxyurea no change compared to control
Downstream Regulation
 Effect of modification (function):  enzymatic activity, induced, molecular association, regulation
 Effect of modification (process):  cell cycle regulation
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
Chk2 (human) Induces
 Comments:  S19A mutant shows impaired dimerization and does not promote Hdmx degradation

S35-p - Chk2 (human) ▲
Orthologous residues
Chk2 (human): S35‑p, Chk2 iso12 (human): S35‑p, Chk2 (mouse): S42‑p, Chk2 (rat): S41‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody
 Relevant cell lines - cell types - tissues:  AT52RM (lymphoblastoid), GM07078 (lymphoblastoid), HCT15 (intestinal), LBC-N
 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
ionizing radiation increase
4-NQO no change compared to control
hydroxyurea no change compared to control
Downstream Regulation
 Effect of modification (function):  enzymatic activity, induced, molecular association, regulation
 Effect of modification (process):  cell cycle regulation
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
Chk2 (human) Induces
 Comments:  S19A mutant shows impaired dimerization and does not promote Hdmx degradation

T68-p - Chk2 (human) ▲
Orthologous residues
Chk2 (human): T68‑p, Chk2 iso12 (human): T68‑p, Chk2 (mouse): T77‑p, Chk2 (rat): T76‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody
 Relevant cell lines - cell types - tissues:  AT52RM (lymphoblastoid), GM07078 (lymphoblastoid), LBC-N
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ATM (human) pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
ionizing radiation increase
hydroxyurea increase
hydroxyurea, caffeine inhibit treatment-induced increase
4-NQO increase
4-NQO, caffeine inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (function):  enzymatic activity, induced
 Comments:  primes Chk2 for activation

T387-p - Chk2 (human) ▲
Orthologous residues
Chk2 (human): T387‑p, Chk2 iso12 (human): T358‑p, Chk2 (mouse): T391‑p, Chk2 (rat): T390‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody
 Relevant cell lines - cell types - tissues:  AT52RM (lymphoblastoid), GM07078 (lymphoblastoid), LBC-N
 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
ionizing radiation increase


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