Curated Information
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Curated Information Page
PubMed Id: 16716194 
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.
Nakaya T, Suzuki T (2006) Role of APP phosphorylation in FE65-dependent gene transactivation mediated by AICD. Genes Cells 11, 633-45 16716194
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T668-p - APP iso2 (mouse)
Orthologous residues
APP (human): T743‑p, APP iso4 (human): T668‑p, APP iso8 (human): T724‑p, APP (mouse): T743‑p, APP iso2 (mouse): T668‑p, APP (rat): T743‑p, APP iso2 (rat): T668‑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), brain, N2a (neuron)
 Cellular systems studied:  cell lines, tissue
 Species studied:  mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
sorbitol JNK1 (mouse) increase
Downstream Regulation
 Effect of modification (function):  intracellular localization, molecular association, regulation
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
Fe65 (mouse) Disrupts intracellular localization transcription, altered microscopy-colocalization
 Comments:  Phosphorylation of APP liberates FE65 from the membrane and then both are independently translocated into the nucleus.


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