Curated Information
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Curated Information Page
PubMed Id: 14523047 
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.
Courtois G, et al. (2003) A hypermorphic IkappaBalpha mutation is associated with autosomal dominant anhidrotic ectodermal dysplasia and T cell immunodeficiency. J Clin Invest 112, 1108-15 14523047
Only sites from this record are displayed on this page. Click on the protein name to open the protein page, and on the RSD number to open the site page. For the complete dataset, click the download button, on the right.
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S32-p - IkB-alpha (human)
Orthologous residues
IkB‑alpha (human): S32‑p, IkB‑alpha (mouse): S32‑p, IkB‑alpha (rat): S32‑p
Characterization
 Methods used to characterize site in vivo electrophoretic mobility shift, mutation of modification site, phospho-antibody
 Relevant cell lines - cell types - tissues:  293T (epithelial), blood, fibroblast-skin, T lymphocyte-blood
 Cellular systems studied:  cell lines, primary cells, primary cultured cells, tissue
 Species studied:  human
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
TNF increase
Downstream Regulation
 Effect of modification (function):  protein degradation
 Effect of modification (process):  transcription, altered

S36-p - IkB-alpha (human)
Orthologous residues
IkB‑alpha (human): S36‑p, IkB‑alpha (mouse): S36‑p, IkB‑alpha (rat): S36‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site
 Relevant cell lines - cell types - tissues:  293T (epithelial)
 Cellular systems studied:  cell lines
 Species studied:  human
Downstream Regulation
 Effect of modification (function):  protein degradation
 Effect of modification (process):  transcription, altered


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