Curated Information
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Home > Curated Information Page > PubMed Id: 10880360
Dowler S, et al. (2000) Phosphoinositide 3-kinase-dependent phosphorylation of the dual adaptor for phosphotyrosine and 3-phosphoinositides by the Src family of tyrosine kinase. Biochem J 349, 605-10 10880360
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, 2015, 43:D512-20). To learn more about the scope of PhosphoSitePlus®, click here.
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Y139-p - DAPP1 (human)
Modsite: kVEEPsIyEsVRVHT SwissProt Entrez-Gene
Orthologous residues
DAPP1 (human): Y139‑p, DAPP1 iso2 (human): Y139‑p, DAPP1 (mouse): Y139‑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)
Cellular systems studied:  cell lines
Species studied:  human
Enzymes shown to modify site in vitro
Type Enzyme
KINASE LYN (human)
KINASE Src (human)
KINASE Lck (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Src (human) pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, transfection of wild-type enzyme, phospho-motif antibody
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
insulin increase
wortmannin insulin inhibit treatment-induced increase
LY294002 insulin inhibit treatment-induced increase
PP2 insulin inhibit treatment-induced increase
PP3 insulin no effect upon treatment-induced increase
IGF-1 increase
wortmannin IGF-1 inhibit treatment-induced increase
LY294002 IGF-1 inhibit treatment-induced increase
IGF-1 PIK3R1 (human) inhibit treatment-induced increase dominant negative
PP2 IGF-1 inhibit treatment-induced increase
EGF increase
wortmannin EGF inhibit treatment-induced increase
LY294002 EGF inhibit treatment-induced increase
PP2 EGF inhibit treatment-induced increase
PIK3CD (human) increase constitutively active
LYN (human) increase
Lck (human) increase