Curated Information
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Curated Information Page
PubMed Id: 12062094 
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.
Humbert S, et al. (2002) The IGF-1/Akt pathway is neuroprotective in Huntington's disease and involves Huntingtin phosphorylation by Akt. Dev Cell 2, 831-7 12062094
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S419-p - Huntingtin (human)
Orthologous residues
Huntingtin (human): S419‑p, Huntingtin (mouse): S398‑p, Huntingtin (rat): S389‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  293T (epithelial)
 Cellular systems studied:  cell lines
 Species studied:  human
 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) genetic transfer of constitutively active upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
IGF-1 increase
LY294002 IGF-1 inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (process):  apoptosis, inhibited


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