Curated Information
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Curated Information Page
PubMed Id: 15192014 
Hu J, Nakano H, Sakurai H, Colburn NH (2004) Insufficient p65 phosphorylation at S536 specifically contributes to the lack of NF-kappaB activation and transformation in resistant JB6 cells. Carcinogenesis 25, 1991-2003 15192014
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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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:  JB (epithelial)
 Cellular systems studied:  cell lines
 Species studied:  mouse
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE IKKB (human)
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
TNF increase
U0126 TNF inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (function):  activity, induced


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