Curated Information
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Curated Information Page
PubMed Id: 14725621 
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.
Rangone H, et al. (2004) The serum- and glucocorticoid-induced kinase SGK inhibits mutant huntingtin-induced toxicity by phosphorylating serine 421 of huntingtin. Eur J Neurosci 19, 273-9 14725621
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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:  'neuron, cortical'-brain, 293T (epithelial)
 Cellular systems studied:  cell lines, primary cultured cells
 Species studied:  human, rat
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE SGK1 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE SGK1 (human) phospho-antibody, transfection of constitutively active enzyme
KINASE Akt1 (human) phospho-antibody, transfection of constitutively active enzyme
Downstream Regulation
 Effect of modification (process):  apoptosis, inhibited


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