Curated Information
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PubMed Id: 15930267 
Palamarchuk A, et al. (2005) Akt phosphorylates Tal1 oncoprotein and inhibits its repressor activity. Cancer Res 65, 4515-9 15930267
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.
Information from this record has been curated, but not yet edited in PhosphoSitePlus® and may be incomplete.
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T90-p - TAL1 (human)
Orthologous residues
TAL1 (human): T90‑p, TAL1 (mouse): T90‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  293 (epithelial), 3T3 (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE Akt1 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Akt1 (human) phospho-antibody, pharmacological inhibitor of upstream enzyme, phospho-motif antibody, co-immunoprecipitation, pharmacological activator of upstream enzyme, transfection of inactive enzyme, transfection of wild-type enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
serum increase
insulin increase
wortmannin insulin inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (process):  translation, induced


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