Curated Information
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Curated Information Page
PubMed Id: 16150728 
Li J, Stern DF (2005) DNA damage regulates Chk2 association with chromatin. J Biol Chem 280, 37948-56 16150728
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, 2012,40:D261-70). To learn more about the scope of PhosphoSitePlus®, click here.
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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
 Relevant cell lines - cell types - tissues:  293 (epithelial), AT22IJE-T (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE Chk2 (human)
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
UV increase
ionizing radiation increase
adriamycin increase
camptothecin increase
AP20187 increase
Downstream Regulation
 Effect of modification (function):  enzymatic activity, induced, intracellular localization, molecular association, regulation
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
Chk2 (human) Induces phosphorylation co-immunoprecipitation, electrophoretic visualization
 Comments:  phosphorylation of T68 induces Chk2 dissociation from chromatin


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