Curated Information
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Curated Information Page
PubMed Id: 18423196 
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.
Imai Y, et al. (2008) Identification of oxidative stress and Toll-like receptor 4 signaling as a key pathway of acute lung injury. Cell 133, 235-49 18423196
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S276-p - NFkB-p65 (mouse)
Orthologous residues
NFkB‑p65 (human): S276‑p, NFkB‑p65 (mouse): S276‑p, NFkB‑p65 (rat): S276‑p
Characterization
 Methods used to characterize site in vivo phospho-antibody
 Relevant cell lines - cell types - tissues:  'macrophage, alveolar'-lung, lung
 Cellular systems studied:  tissue
 Species studied:  mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
injury increase acid-induced lung injury
injury TLR4 (mouse) inhibit treatment-induced increase homozygous null
injury TRAF6 (mouse) inhibit treatment-induced increase homozygous null
injury TICAM1 (mouse) inhibit treatment-induced increase homozygous null
virus infection increase H5N1 avian flu
virus infection TLR4 (mouse) inhibit treatment-induced increase homozygous null
virus infection TICAM1 (mouse) inhibit treatment-induced increase homozygous null


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