Curated Information
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Curated Information Page
PubMed Id: 11877376 
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.
Kim ST, Xu B, Kastan MB (2002) Involvement of the cohesin protein, Smc1, in Atm-dependent and independent responses to DNA damage. Genes Dev 16, 560-70 11877376
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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S957-p - Smc1 (human)
Orthologous residues
Smc1 (human): S957‑p, Smc1 (mouse): S957‑p, Smc1 (rat): S957‑p
Characterization
 Methods used to characterize site in vivo electrophoretic mobility shift, phospho-antibody
 Disease tissue studied:  ataxia-telangiectasic cancer
 Relevant cell lines - cell types - tissues:  GM01526 (fibroblast), GM0536 (fibroblast), GM0637 (fibroblast), GM09607 (fibroblast)
 Cellular systems studied:  cell lines, primary cultured cells
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE ATM (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ATM (human) transfection of wild-type 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
UV increase
hydroxyurea increase
Downstream Regulation
 Effect of modification (process):  cell cycle regulation
 Comments:  S957A and S966A mutations inhibited the S phase checkpoint in two different cell types.

S966-p - Smc1 (human)
Orthologous residues
Smc1 (human): S966‑p, Smc1 (mouse): S966‑p, Smc1 (rat): S966‑p
Characterization
 Methods used to characterize site in vivo electrophoretic mobility shift, phospho-antibody
 Disease tissue studied:  ataxia-telangiectasic cancer
 Relevant cell lines - cell types - tissues:  GM01526 (fibroblast), GM0536 (fibroblast), GM0637 (fibroblast), GM09607 (fibroblast)
 Cellular systems studied:  cell lines, primary cultured cells
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE ATM (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ATM (human) transfection of wild-type 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
UV increase
hydroxyurea increase
Downstream Regulation
 Effect of modification (process):  cell cycle regulation
 Comments:  S957A and S966A mutations inhibited the S phase checkpoint in two different cell types.


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