Curated Information
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Curated Information Page
PubMed Id: 15084259 
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.
Information from this record has been curated, but not yet edited in PhosphoSitePlus® and may be incomplete.
Seoane J, et al. (2004) Integration of Smad and forkhead pathways in the control of neuroepithelial and glioblastoma cell proliferation. Cell 117, 211-23 15084259
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S473-p - Akt1 (human)
Orthologous residues
Akt1 (human): S473‑p, Akt1 (mouse): S473‑p, Akt1 (rat): S473‑p, Akt1 (fruit fly): S586‑p, Akt1 (cow): S473‑p
Characterization
 Methods used to characterize site in vivo phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  HaCaT (keratinocyte)
 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
TGF-beta increase
LY294002 TGF-beta inhibit treatment-induced increase
IGF-1 TGF-beta augment treatment-induced increase
LY294002 decrease
IGF-1 increase


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