Curated Information
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Curated Information Page
PubMed Id: 12842894 
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.
Sakurai H, et al. (2003) Tumor necrosis factor-alpha-induced IKK phosphorylation of NF-kappaB p65 on serine 536 is mediated through the TRAF2, TRAF5, and TAK1 signaling pathway. J Biol Chem 278, 36916-23 12842894
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S536-p - NFkB-p65 (human)
Orthologous residues
NFkB‑p65 (human): S536‑p, NFkB‑p65 (mouse): S534‑p, NFkB‑p65 (rat): S535‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  293 (epithelial), HeLa (cervical), Jurkat (T lymphocyte), MEF (fibroblast) [IGF1R (mouse)], RAW 264 (macrophage)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
IL-1b increase
LPS increase
A23187, phorbol ester increase
TNF increase
LLnL TNF augment treatment-induced increase
calyculin A TNF augment treatment-induced increase
Bay 11-7082 TNF inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (function):  activity, induced


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