Curated Information
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Curated Information Page
PubMed Id: 16377563 
Stucki M, et al. (2005) MDC1 directly binds phosphorylated histone H2AX to regulate cellular responses to DNA double-strand breaks. Cell 123, 1213-26 16377563
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.
Information from this record has been curated, but not yet edited in PhosphoSitePlus® and may be incomplete.
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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T137-p - H2AX (human)
Orthologous residues
H2AX (human): T137‑p, H2AX (mouse): S137‑p, H2AX (rat): S137‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  MEF (fibroblast), U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
 Comments:  MEFs were H2AX -/- p53 -/-
Downstream Regulation
 Effect of modification (function):  intracellular localization
 Comments:  T136A,S139A did not localize to MDC1 IRIF nuclear foci and did not complement the null.

S140-p - H2AX (human)
Orthologous residues
H2AX (human): S140‑p, H2AX (mouse): S140‑p, H2AX (rat): S140‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  MEF (fibroblast), U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
 Comments:  MEFs were H2AX -/- p53 -/-
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
ionizing radiation increase
siRNA ionizing radiation inhibit treatment-induced increase MDC1 shRNA. Increases kinetics of dephosphorylation.
ionizing radiation inhibit treatment-induced increase ATM/DNA-PKcs inhibitors
Downstream Regulation
 Effect of modification (function):  intracellular localization, molecular association, regulation
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
MDC1 (human) BRCT Induces pull-down assay
PARP1 (human) Induces pull-down assay
Rad50 (human) Induces pull-down assay
NBS1 (human) Induces pull-down assay
 Comments:  T136A,S139A did not localize to MDC1 IRIF nuclear foci and did not complement the null.


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