Curated Information
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PubMed Id: 17189255 
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.
Information from this record has been curated, but not yet edited in PhosphoSitePlus® and may be incomplete.
Chen BP, et al. (2007) Ataxia telangiectasia mutated (ATM) is essential for DNA-PKcs phosphorylations at the Thr-2609 cluster upon DNA double strand break. J Biol Chem 282, 6582-7 17189255
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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S2056-p - DNA-PK (human) ▲
Orthologous residues
DNA‑PK (human): S2056‑p, DNA‑PK (mouse): S2053‑p, DNA‑PK (rat): S2051‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  ataxia-telangiectasia, breast cancer
 Relevant cell lines - cell types - tissues:  CHO (fibroblast), GM02052 (fibroblast), HeLa (cervical), HSF (fibroblast), L3 (lymphoblastoid), MCF-7 (breast cell)
 Cellular systems studied:  cell lines
 Species studied:  hamster, human
 Comments:  BT human lymphoblastoid cell line, AT5 (SV-40 transformed A-T cells), 1BR3 human fibroblasts
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE DNA-PK (human) pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody, modification site within consensus motif
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
ionizing radiation increase
siRNA ionizing radiation ATM (human) no effect upon treatment-induced increase
KU-55933 ionizing radiation no effect upon treatment-induced increase
NU7441 ionizing radiation inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (process):  cell growth, altered, chromatin organization, altered
 Comments:  increases survival in ionizing radiation and repairing double strand DNA breaks

T2609-p - DNA-PK (human) ▲
Orthologous residues
DNA‑PK (human): T2609‑p, DNA‑PK (mouse): T2605‑p, DNA‑PK (rat): T2603‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  ataxia-telangiectasia, breast cancer
 Relevant cell lines - cell types - tissues:  CHO (fibroblast), GM02052 (fibroblast), HeLa (cervical), HSF (fibroblast), L3 (lymphoblastoid), MCF-7 (breast cell)
 Cellular systems studied:  cell lines
 Species studied:  hamster, human
 Comments:  BT human lymphoblastoid cell line, AT5 (SV-40 transformed A-T cells), 1BR3 human fibroblasts
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ATM (human) pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody, modification site within consensus motif, siRNA inhibition of 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
siRNA ionizing radiation ATM (human) inhibit treatment-induced increase
KU-55933 ionizing radiation inhibit treatment-induced increase
NU7441 ionizing radiation no effect upon treatment-induced increase
Downstream Regulation
 Effect of modification (process):  cell growth, altered, chromatin organization, altered
 Comments:  increases survival in ionizing radiation and repairing double strand DNA breaks

S2612-p - DNA-PK (human) ▲
Orthologous residues
DNA‑PK (human): S2612‑p, DNA‑PK (mouse): S2608‑p, DNA‑PK (rat): F2606‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  CHO (fibroblast), HeLa (cervical)
 Cellular systems studied:  cell lines
 Species studied:  hamster, human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ATM (human) pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody, modification site within consensus motif, siRNA inhibition of 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
KU-55933 ionizing radiation inhibit treatment-induced increase
NU7441 ionizing radiation no effect upon treatment-induced increase
Downstream Regulation
 Effect of modification (process):  cell growth, altered, chromatin organization, altered
 Comments:  increases survival in ionizing radiation and repairing double strand DNA breaks

T2638-p - DNA-PK (human) ▲
Orthologous residues
DNA‑PK (human): T2638‑p, DNA‑PK (mouse): T2634‑p, DNA‑PK (rat): T2632‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  CHO (fibroblast), HeLa (cervical)
 Cellular systems studied:  cell lines
 Species studied:  hamster, human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ATM (human) pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody, modification site within consensus motif, siRNA inhibition of 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
KU-55933 ionizing radiation inhibit treatment-induced increase
NU7441 ionizing radiation no effect upon treatment-induced increase
Downstream Regulation
 Effect of modification (process):  cell growth, altered, chromatin organization, altered
 Comments:  increases survival in ionizing radiation and repairing double strand DNA breaks

T2647-p - DNA-PK (human) ▲
Orthologous residues
DNA‑PK (human): T2647‑p, DNA‑PK (mouse): T2643‑p, DNA‑PK (rat): T2641‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  ataxia-telangiectasia, breast cancer
 Relevant cell lines - cell types - tissues:  CHO (fibroblast), GM02052 (fibroblast), HeLa (cervical), HSF (fibroblast), L3 (lymphoblastoid), MCF-7 (breast cell)
 Cellular systems studied:  cell lines
 Species studied:  hamster, human
 Comments:  BT human lymphoblastoid cell line, AT5 (SV-40 transformed A-T cells), 1BR3 human fibroblasts
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ATM (human) pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody, modification site within consensus motif, siRNA inhibition of 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
siRNA ionizing radiation ATM (human) inhibit treatment-induced increase
KU-55933 ionizing radiation inhibit treatment-induced increase
NU7441 ionizing radiation no effect upon treatment-induced increase
Downstream Regulation
 Effect of modification (process):  cell growth, altered, chromatin organization, altered
 Comments:  increases survival in ionizing radiation and repairing double strand DNA breaks


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