Curated Information
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Curated Information Page
PubMed Id: 18772195 
Zala D, et al. (2008) Phosphorylation of mutant huntingtin at S421 restores anterograde and retrograde transport in neurons. Hum Mol Genet 17, 3837-46 18772195
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, 2012,40:D261-70). To learn more about the scope of PhosphoSitePlus®, click here.
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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, western blotting
 Relevant cell lines - cell types - tissues:  'neuron, cortical'-brain, 293 (epithelial)
 Cellular systems studied:  cell lines, primary cells
 Species studied:  mouse
 Comments:  neurons from wt or 109Q mutant (having a CAG expansion inserted into endogenous huntingtin gene) mice
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
IGF-1 increase
Downstream Regulation
 Effect of modification (function):  activity, induced, molecular association, regulation
 Effect of modification (process):  cytoskeletal reorganization
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
dynactin 1 (human) Induces molecular association, regulation co-immunoprecipitation
 Comments:  vesicular transport of BDNF in axons
Associated Diseases
Diseases: Alterations: Comments:
Huntington's disease decreased phosphorylation decreased in HD; experimental phosphorylation restores defects in function


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