Curated Information
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Curated Information Page
PubMed Id: 10802669 
Gatei M, et al. (2000) ATM-dependent phosphorylation of nibrin in response to radiation exposure. Nat Genet 25, 115-9 10802669
This page summarizes selected information from the record 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.
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S343-p - NBS1 (human)
Orthologous residues
NBS1 (human): S343‑p, NBS1 (mouse): S343‑p, NBS1 (rat): S343‑p
 Methods used to characterize site in vivo electrophoretic mobility shift, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  ataxia-telangiectasia
 Relevant cell lines - cell types - tissues:  AT1ABR (lymphoblastoid), AT3ABR (lymphoblastoid), C2ABR (lymphoblastoid), C30ABR (lymphoblastoid), C3ABR (lymphoblastoid), L3 (lymphoblastoid)
 Cellular systems studied:  cell lines
 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) co-immunoprecipitation, pharmacological activator of upstream enzyme, genetic knockout/knockin of upstream enzyme, electrophoretic mobility shift, phospho-antibody, genetic transfer of inducible upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
wortmannin no change compared to control
ionizing radiation increase
Downstream Regulation
 Effect of modification (function):  activity, induced
 Effect of modification (process):  cell growth, altered
 Comments:  more cell survival after ionizing radiation

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