Curated Information
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Curated Information Page
PubMed Id: 19406989 
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.
Terme JM, Lhermitte L, Asnafi V, Jalinot P (2009) TGF-beta induces degradation of TAL1/SCL by the ubiquitin-proteasome pathway through AKT-mediated phosphorylation. Blood 113, 6695-8 19406989
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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 immunoprecipitation, mutation of modification site, western blotting
 Relevant cell lines - cell types - tissues:  HeLa (cervical)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Akt1 (human) transfection of wild-type enzyme, transfection of inactive enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
TGF-beta increase
wortmannin TGF-beta inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (function):  molecular association, regulation, protein degradation, ubiquitination
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
CHIP (human) Induces co-immunoprecipitation


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