Curated Information
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Home > Curated Information Page > PubMed Id: 10724175
Lee JS, et al. (2000) hCds1-mediated phosphorylation of BRCA1 regulates the DNA damage response. Nature 404, 201-4 10724175
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, 2015, 43:D512-20). To learn more about the scope of PhosphoSitePlus®, click here.
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S988-p - BRCA1 (human)
Modsite: PPLFPIksFVKTKCK SwissProt Entrez-Gene
Orthologous residues
BRCA1 (human): S988‑p, BRCA1 iso6 (human): , BRCA1 iso7 (human): S988‑p, BRCA1 (mouse): S971‑p, BRCA1 (rat): S975‑p
Characterization
Methods used to characterize site in vivo microscopy-colocalization with upstream kinase, mutation of modification site, phospho-antibody
Relevant cell lines - cell types - tissues:  HCC1937 (breast cell), HEK293T (epithelial), MCF-7 (breast cell)
Cellular systems studied:  cell lines
Species studied:  human
Enzymes shown to modify site in vitro
Type Enzyme
KINASE Chk2 (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Chk2 (human) co-immunoprecipitation, transfection of inactive enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
ionizing_radiation increase
Downstream Regulation
Effect of modification (function):  intracellular localization
Comments:  Colocalized BRCA1 and Chk2 separate after phosphorylation of both. Phosphorylation at S988 increases survival 8 days after irradiation.