Curated Information
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Curated Information Page
PubMed Id: 18332866 
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.
Gehen SC, et al. (2008) hSMG-1 and ATM sequentially and independently regulate the G1 checkpoint during oxidative stress. Oncogene 27, 4065-74 18332866
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, western blotting
 Disease tissue studied:  ataxia-telangiectasia, colorectal cancer, colorectal carcinoma, lung cancer
 Relevant cell lines - cell types - tissues:  A549 (pulmonary), GM00536 (fibroblast), GM01526 (fibroblast), HCT116 (intestinal)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
hyperoxia increase
hyperoxia ATM (human) inhibit treatment-induced increase null cells

S15-p - p53 (human) ▲
Orthologous residues
p53 (human): S15‑p, p53 (mouse): S15‑p, p53 iso2 (mouse): S18‑p, p53 (rat): S15‑p, p53 (rabbit): S15‑p, p53 (monkey): S15‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Disease tissue studied:  ataxia-telangiectasia, colorectal cancer, colorectal carcinoma, lung cancer
 Relevant cell lines - cell types - tissues:  A549 (pulmonary), GM00536 (fibroblast), GM01526 (fibroblast), HCT116 (intestinal)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE SMG1 (human) genetic knockout/knockin of upstream enzyme, siRNA inhibition of enzyme responsible for rapid, early phosphorylation
KINASE ATM (human) genetic knockout/knockin of upstream enzyme, siRNA inhibition of enzyme maintains later phosphorylation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
hyperoxia increase
wortmannin hyperoxia inhibit treatment-induced increase
siRNA hyperoxia inhibit treatment-induced increase SMG1 siRNA
siRNA hyperoxia inhibit treatment-induced increase ATM siRNA; at later time points


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