Curated Information
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Curated Information Page
PubMed Id: 12447382 
DiTullio RA, et al. (2002) 53BP1 functions in an ATM-dependent checkpoint pathway that is constitutively activated in human cancer. Nat Cell Biol 4, 998-1002 12447382
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.
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 phospho-antibody
 Disease tissue studied:  breast cancer, lung cancer
 Relevant cell lines - cell types - tissues:  Saos-2 (bone cell), SKNSH (neural crest), SW480 (intestinal), U2OS (bone cell) [GR (human)]
 Cellular systems studied:  tissue
 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

S966-p - Smc1 (human)
Orthologous residues
Smc1 (human): S966‑p, Smc1 (mouse): S966‑p, Smc1 (rat): S966‑p
Characterization
 Methods used to characterize site in vivo phospho-antibody
 Disease tissue studied:  ataxia-telangiectasic cancer
 Relevant cell lines - cell types - tissues:  AG1522 (fibroblast), SKNSH (neural crest)
 Cellular systems studied:  primary cultured cells
 Species studied:  human
 Comments:  AT5BI fibroblasts were derived from a patient with ataxia telangiectasia.
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ATM (human) Cells from ataxia telangiectasia patients, deficient in ATM activity, failed to phosphorylate S966 after ionizing radiation.
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
ionizing radiation increase
Associated Diseases
Diseases: Alterations: Comments:
ataxia-telangiectasic cancer decreased


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