Curated Information
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Curated Information Page
PubMed Id: 15533933 
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.
Helt CE, et al. (2005) Ataxia telangiectasia mutated (ATM) and ATM and Rad3-related protein exhibit selective target specificities in response to different forms of DNA damage. J Biol Chem 280, 1186-92 15533933
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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S345-p - Chk1 (human) ▲
Orthologous residues
Chk1 (human): S345‑p, Chk1 (mouse): S345‑p, Chk1 (rat): S345‑p, Chk1 (chicken): S345‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody
 Disease tissue studied:  ataxia-telangiectasia, lung cancer, non-small cell lung cancer
 Relevant cell lines - cell types - tissues:  A549 (pulmonary), GM00536 (fibroblast), GM01526 (fibroblast), NCI-H1299 (pulmonary), U2OS (bone cell) [GR (human)]
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ATR (human) activation of upstream enzyme, transfection of dominant-negative enzyme
KINASE ATM (human) genetic knockout/knockin of upstream enzyme, activation of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
ionizing radiation increase
doxycycline ionizing radiation inhibit treatment-induced increase
UV increase
doxycycline UV inhibit treatment-induced increase

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:  ataxia-telangiectasia, lung cancer, non-small cell lung cancer
 Relevant cell lines - cell types - tissues:  A549 (pulmonary), GM00536 (fibroblast), GM01526 (fibroblast), NCI-H1299 (pulmonary), U2OS (bone cell) [GR (human)]
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ATR (human) activation of upstream enzyme, transfection of dominant-negative enzyme
KINASE ATM (human) genetic knockout/knockin of upstream enzyme, activation of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
ionizing radiation increase
doxycycline ionizing radiation inhibit treatment-induced increase
UV increase
doxycycline UV inhibit treatment-induced increase

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
 Disease tissue studied:  ataxia-telangiectasia, lung cancer, non-small cell lung cancer
 Relevant cell lines - cell types - tissues:  A549 (pulmonary), GM00536 (fibroblast), GM01526 (fibroblast), NCI-H1299 (pulmonary), U2OS (bone cell) [GR (human)]
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ATR (human) activation of upstream enzyme, transfection of dominant-negative enzyme
KINASE ATM (human) genetic knockout/knockin of upstream enzyme, activation of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
ionizing radiation increase
doxycycline ionizing radiation inhibit treatment-induced increase
UV increase
doxycycline UV inhibit treatment-induced increase


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