Curated Information
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Curated Information Page
PubMed Id: 15073167 
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.
Yeh PY, et al. (2004) Suppression of MEK/ERK signaling pathway enhances cisplatin-induced NF-kappaB activation by protein phosphatase 4-mediated NF-kappaB p65 Thr dephosphorylation. J Biol Chem 279, 26143-8 15073167
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T435-p - NFkB-p65 (human)
Orthologous residues
NFkB‑p65 (human): T435‑p, NFkB‑p65 (mouse): T433‑p, NFkB‑p65 (rat): T434‑p
Characterization
 Methods used to characterize site in vivo electrophoretic mobility shift, mutation of modification site, phospho-antibody, phosphoamino acid analysis, western blotting
 Disease tissue studied:  cervical cancer, cervical squamous cell carcinoma
 Relevant cell lines - cell types - tissues:  SiHa (squamous)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
PHOSPHATASE PPP4C (human) phospho-motif antibody, antisense inhibition of upstream enzyme, transfection of wild-type enzyme, pharmacological activator of upstream enzyme, co-immunoprecipitation


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