Curated Information
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Curated Information Page
PubMed Id: 11313464 
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.
Kim DW, Cochran BH (2001) JAK2 activates TFII-I and regulates its interaction with extracellular signal-regulated kinase. Mol Cell Biol 21, 3387-97 11313464
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Y248-p - GTF2I iso2 (human)
Orthologous residues
GTF2I (human): Y248‑p, GTF2I iso2 (human): Y248‑p, GTF2I (mouse): Y248‑p, GTF2I iso8 (mouse): Y248‑p, GTF2I (rat): Y248‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  3T3 (fibroblast) [SHP-2 (mouse), homozygous knockout]
 Cellular systems studied:  cell lines
 Species studied:  mouse
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE JAK2 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE JAK2 (human) transfection of wild-type enzyme, transfection of inactive enzyme, inhibition of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
serum increase
AG490 serum inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Effect of modification (process):  transcription, altered
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
ERK1 (human) Induces


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