Curated Information

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Curated Information Page

PubMed Id: 12447382

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.

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

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.

T68-p - Chk2 (human)

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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)

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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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