Curated Information
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Curated Information Page
PubMed Id: 15668230 
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.
Li J, Stern DF (2005) Regulation of CHK2 by DNA-dependent protein kinase. J Biol Chem 280, 12041-50 15668230
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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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 electrophoretic mobility shift, phospho-antibody, western blotting
 Disease tissue studied:  ataxia-telangiectasia, brain cancer, glioblastoma, glioma, Nijmegen Breakage Syndrome
 Relevant cell lines - cell types - tissues:  293 (epithelial), CHO (fibroblast), fibroblast, M059J (glial), M059K (glial)
 Cellular systems studied:  cell lines
 Species studied:  hamster, human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE DNAPK (human)
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
ionizing radiation increase
rapamycin ionizing radiation no effect upon treatment-induced increase
DNA-PK inhibitor II ionizing radiation inhibit treatment-induced increase
camptothecin increase

T383-p - Chk2 (human)
Orthologous residues
Chk2 (human): T383‑p, Chk2 iso12 (human): T354‑p, Chk2 (mouse): T387‑p, Chk2 (rat): T386‑p
Characterization
 Methods used to characterize site in vivo electrophoretic mobility shift, phospho-antibody, western blotting
 Disease tissue studied:  ataxia-telangiectasia, brain cancer, glioblastoma, glioma, Nijmegen Breakage Syndrome
 Relevant cell lines - cell types - tissues:  293 (epithelial), CHO (fibroblast), fibroblast, M059J (glial), M059K (glial)
 Cellular systems studied:  cell lines
 Species studied:  hamster, human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE DNAPK (human)
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
ionizing radiation increase
camptothecin increase

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 electrophoretic mobility shift, phospho-antibody, western blotting
 Disease tissue studied:  ataxia-telangiectasia, brain cancer, glioblastoma, glioma, Nijmegen Breakage Syndrome
 Relevant cell lines - cell types - tissues:  293 (epithelial), CHO (fibroblast), fibroblast, M059J (glial), M059K (glial)
 Cellular systems studied:  cell lines
 Species studied:  hamster, human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE DNAPK (human)
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
ionizing radiation increase
camptothecin increase


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