Curated Information
Javascript is not enabled on this browser. This site will not work properly without Javascript.
PhosphoSitePlus Homepage Cell Signaling Technology
HomeAbout PhosphoSiteUsing PhosphoSiteCuration ProcessContact
NIH-logos NIGMS Logo NIAAA Logo NCI Logo NIH Logo
Curated Information Page
PubMed Id: 11684015 
Slupianek A, et al. (2001) BCR/ABL regulates mammalian RecA homologs, resulting in drug resistance. Mol Cell 8, 795-806 11684015
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.
Download Sites

Y315-p - RAD51 (human)
Orthologous residues
RAD51 (human): Y315‑p, RAD51 (mouse): Y315‑p, RAD51 (rat): Y315‑p
 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-ABL1 (human) transfection of inactive enzyme, co-immunoprecipitation, microscopy-colocalization, phospho-antibody, transfection of wild-type enzyme
Downstream Regulation
 Effect of modification (process):  apoptosis, altered
 Comments:  controls resistance to cisplatin and mitomycin C

Home  |  Curator Login With enhanced literature mining using Linguamatics I2E I2E Logo Produced by 3rd Millennium  |  Design by Digizyme
©2003-2013 Cell Signaling Technology, Inc.