Curated Information

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Curated Information Page

PubMed Id: 15677476

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.

Chen BP, et al. (2005) Cell cycle dependence of DNA-dependent protein kinase phosphorylation in response to DNA double strand breaks. J Biol Chem 280, 14709-15 15677476

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.

S2056-p - DNAPK (human)

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Orthologous residues

DNAPK (human): S2056‑p, DNAPK (mouse): S2053‑p, DNAPK (rat): S2051‑p

Characterization

Methods used to characterize site in vivo: phospho-antibody, western blotting

Disease tissue studied: brain cancer, glioblastoma, glioma

Relevant cell lines - cell types - tissues: CHO (fibroblast), HSF (fibroblast), M059J (glial), M059K (glial)

Cellular systems studied: cell lines

Species studied: hamster, human

Upstream Regulation

Potential in vivo enzymes for site:

Type	Enzyme	Evidence	Notes
KINASE	DNAPK (human)	transfection of inactive enzyme, transfection of wild-type enzyme

Treatments, proteins and their effect on site modification:

Treatments	Referenced Treatments	Effect
bleomycin		increase
ionizing radiation		increase
wortmannin	ionizing radiation	inhibit treatment-induced increase
etoposide		increase
camptothecin		increase
aphidicolin	camptothecin	inhibit treatment-induced increase
aphidicolin		decrease

T2609-p - DNAPK (human)

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