Curated Information
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Curated Information Page
PubMed Id: 21996732 
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.
Shih MC, et al. (2012) TOPK/PBK promotes cell migration via modulation of the PI3K/PTEN/AKT pathway and is associated with poor prognosis in lung cancer. Oncogene 31, 2389-400 21996732
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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
 Disease tissue studied:  lung cancer, non-small cell lung cancer
 Relevant cell lines - cell types - tissues:  A549 (pulmonary), CL1-0 (pulmonary), IMR-90 (fibroblast), NCI-H1299 (pulmonary), NCI-H23 (pulmonary)
 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
PBK (human) increase WT PBK increase, inactive kinase inhibits, PBK siRNA inhibits
LY294002 decrease


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