Lipopolysaccharide-induced NF-κB nuclear translocation is primarily dependent on MyD88, but TNF$\alpha$ expression requires TRIF and MyD88
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TLR4 signalling through the MyD88 and TRIF-dependent pathways initiates translocation of the transcription factor NF-κB into the nucleus. In cell population studies using mathematical modeling and functional analyses, Cheng et al. suggested that LPS-driven activation of MyD88, in the absence of TRIF, impairs NF-κB translocation. We tested the model proposed by Cheng et al. using real-time single cell analysis in macrophages expressing EGFP-tagged p65 and a TNF
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2045-2322
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Biotechnology and Biological Sciences Research Council (BB/K006436/1)
Medical Research Council (G1000133)
Wellcome Trust (108045/Z/15/Z)