Curated Information
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Curated Information Page
PubMed Id: 15800615 
Esashi F, et al. (2005) CDK-dependent phosphorylation of BRCA2 as a regulatory mechanism for recombinational repair. Nature 434, 598-604 15800615
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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S3291-p - BRCA2 (human)
Orthologous residues
BRCA2 (human): S3291‑p, BRCA2 (mouse): S3214‑p, BRCA2 (rat): S3222‑p
 Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  fibrosarcoma of soft tissue
 Relevant cell lines - cell types - tissues:  HeLa (cervical), HT1080 (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
nocodazole increase
ionizing radiation decrease
ionizing radiation ATM (human) inhibit treatment-induced decrease deficient cells
roscovitine decrease
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Effect of modification (process):  cell cycle regulation
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
RAD51 (human) Disrupts pull-down assay
 Comments:  double-strand break repair efficiency
Associated Diseases
Diseases: Alterations: Comments:
breast cancer mutation of site

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