Curated Information
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Curated Information Page
PubMed Id: 10973490 
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.
Matsuoka S, et al. (2000) Ataxia telangiectasia-mutated phosphorylates Chk2 in vivo and in vitro. Proc Natl Acad Sci U S A 97, 10389-94 10973490
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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:  mutation of modification site, phospho-antibody
 Relevant cell lines - cell types - tissues:  293T (epithelial), MEF (fibroblast) [IGF1R (mouse)]
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE ATM (human)
KINASE ATR (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ATM (human) transfection of wild-type enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
ionizing radiation increase
UV increase
hydroxyurea increase


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