Curated Information
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Curated Information Page
PubMed Id: 17018862 
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.
Yoshida C, et al. (2007) Bcr-Abl signaling through the PI-3/S6 kinase pathway inhibits nuclear translocation of the transcription factor Bach2, which represses the antiapoptotic factor heme oxygenase-1. Blood 109, 1211-9 17018862
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S521-p - BACH2 (human)
Orthologous residues
BACH2 (human): S521‑p, BACH2 (mouse): S520‑p, BACH2 iso2 (mouse):
Characterization
 Methods used to characterize site in vivo mutation of modification site
 Relevant cell lines - cell types - tissues:  3T3 (fibroblast) [SHP-2 (mouse), homozygous knockout]
 Cellular systems studied:  cell lines
 Species studied:  mouse
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE p70S6K (human) pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
LY294002 decrease
Downstream Regulation
 Effect of modification (function):  intracellular localization
 Effect of modification (process):  apoptosis, inhibited, cell growth, altered, transcription, altered
 Comments:  regulates transcription of HO-1


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