Curated Information
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Curated Information Page
PubMed Id: 11684015 
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.
Slupianek A, et al. (2001) BCR/ABL regulates mammalian RecA homologs, resulting in drug resistance. Mol Cell 8, 795-806 11684015
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Y315-p - Rad51 (human)
Orthologous residues
Rad51 (human): Y315‑p, Rad51 (mouse): Y315‑p, Rad51 (rat): Y315‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  32D (myeloid), COS (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  monkey, mouse
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Bcr/Abl (human) phospho-antibody, microscopy-colocalization, co-immunoprecipitation, transfection of inactive enzyme, transfection of wild-type enzyme
Downstream Regulation
 Effect of modification (process):  apoptosis, altered
 Comments:  controls resistance to cisplatin and mitomycin C


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