Curated Information
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Curated Information Page
PubMed Id: 17101782 
Tan Y, Raychaudhuri P, Costa RH (2007) Chk2 mediates stabilization of the FoxM1 transcription factor to stimulate expression of DNA repair genes. Mol Cell Biol 27, 1007-16 17101782
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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S361-p - FOXM1 iso2 (human)
Orthologous residues
FOXM1 (human): S376‑p, FOXM1 iso2 (human): S361‑p, FOXM1 (mouse): S374‑p
Characterization
 Methods used to characterize site in vivo immunoprecipitation, mutation of modification site, phospho-antibody
 Relevant cell lines - cell types - tissues:  U2OS (bone cell) [GR (human)]
 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) pharmacological activator of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
etoposide increase
ionizing radiation increase
Downstream Regulation
 Effect of modification (function):  protein stabilization
 Effect of modification (process):  transcription, induced
 Comments:  plays a role in the DNA damage/checkpoint signaling


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