Curated Information
Javascript is not enabled on this browser. This site will not work properly without Javascript.
PhosphoSitePlus Homepage Cell Signaling Technology
PhosphoSitePlus
HomeAbout PhosphoSiteUsing PhosphoSiteCuration ProcessContact
NIH-logos NIGMS Logo NIAAA Logo NCI Logo NIH Logo
Curated Information Page
PubMed Id: 12741986 
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.
Emamian ES, et al. (2003) Serine 776 of ataxin-1 is critical for polyglutamine-induced disease in SCA1 transgenic mice. Neuron 38, 375-87 12741986
Download Sites

S775-p - ataxin-1 (human)
Orthologous residues
ataxin‑1 (human): S775‑p, ataxin‑1 (mouse): S751‑p, ataxin‑1 (rat): S749‑p
Characterization
 Methods used to characterize site in vivo [32P] bio-synthetic labeling, mass spectrometry, mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  'neuron, Purkinje'-'brain, cerebellum', CHO (fibroblast) [EphB1 (human), transfection], COS (fibroblast)
 Cellular systems studied:  cell lines, primary cells
 Species studied:  hamster, monkey, mouse
Downstream Regulation
 Effect of modification (function):  intracellular localization
 Effect of modification (process):  cytoskeletal reorganization
 Comments:  ataxin-1 S776A mutant reduces nuclear inclusion bodies of ataxin-1 in B05 tg/+ mice.
Associated Diseases
Diseases: Alterations: Comments:
spinocerebellar ataxia type 1 increased


Home  |  Curator Login With enhanced literature mining using Linguamatics I2E I2E Logo Produced by 3rd Millennium  |  Design by Digizyme
©2003-2013 Cell Signaling Technology, Inc.