Curated Information
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Curated Information Page
PubMed Id: 11418864 
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.
Bao S, et al. (2001) ATR/ATM-mediated phosphorylation of human Rad17 is required for genotoxic stress responses. Nature 411, 969-74 11418864
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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S646-p - Rad17 (human) ▲
Orthologous residues
Rad17 (human): S646‑p, Rad17 (mouse): S647‑p
Characterization
 Methods used to characterize site in vivo:  [32P] bio-synthetic labeling, immunoprecipitation, mutation of modification site, phospho-antibody
 Relevant cell lines - cell types - tissues:  293T (epithelial), A549 (pulmonary), GM847 (fibroblast), MCF-7 (breast cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE ATR (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ATM (human) genetic knockout/knockin of upstream enzyme
KINASE ATR (human) transfection of inactive enzyme
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Effect of modification (process):  cell cycle regulation
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
RAD1 (human) Induces
 Comments:  required for interaction with Rad1 and activation of the G2 checkpoint in cells damaged by ionizing radiation

S656-p - Rad17 (human) ▲
Orthologous residues
Rad17 (human): S656‑p, Rad17 (mouse): S657‑p
Characterization
 Methods used to characterize site in vivo:  [32P] bio-synthetic labeling, immunoprecipitation, mutation of modification site, phospho-antibody
 Relevant cell lines - cell types - tissues:  293T (epithelial), A549 (pulmonary), GM847 (fibroblast), MCF-7 (breast cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE ATR (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ATM (human) genetic knockout/knockin of upstream enzyme
KINASE ATR (human) transfection of inactive enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
UV increase
ionizing radiation increase
hydroxyurea increase
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Effect of modification (process):  cell cycle regulation
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
RAD1 (human) Induces
 Comments:  required for interaction with Rad1 and activation of the G2 checkpoint in cells damaged by ionizing radiation


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