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ingest and kill the pathogenic organism, digest its proteins into small peptide ... messenger signalling molecule that remains tethered to the lipid bilayer [21].
Apr 15, 2017 - Print ISSN: 0022-1767 Online ISSN: 1550-6606. .... Department of Pharmacy and Pharmacology, Bath University, Bath, United Kingdom.
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Feb 2, 2010 - also directly stimulates class IA phosphoinositide 3-kinase (PI3K) ... focus for designing selective inhibitors targeting specific diseases.
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1995; Villain et al. 1996). In addition, a GT element called site 1 (GT-1), found in the ribosomal protein gene rps1 promoter, has been shown to repress tran-.
HL60 and EL4 cells incubated with tumor necrosis factor-a (TNF-a) plus staurosporin, a potent inhibitor of protein kinases, showed at least S-fold increased.
Receive free email-alerts when new articles cite this article. Sign up at: ... TLR5 signaling is independent of Toll-IL-1R domain-containing adapter protein (8).
The Journal of Immunology
TLR5-Mediated Phosphoinositide 3-Kinase Activation Negatively Regulates Flagellin-Induced Proinflammatory Gene Expression1 Yimin Yu,* Shigenori Nagai,†‡ Huixia Wu,* Andrew S. Neish,* Shigeo Koyasu,†‡ and Andrew T. Gewirtz2* Epithelial cells detect motile pathogens via TLR5 ligation of flagellin, resulting in rapid induction of antibacterial/proinflammatory gene expression. Although such flagellin-induced gene expression is quite transient, likely to avoid the negative consequences of inflammation, little is known regarding the molecular mechanisms that mediate its shutdown. We hypothesized that, analogous to the case for TLR4, phosphoinositide 3-kinase (PI3K) might negatively regulate TLR5 signaling. However, because PI3K is an essential positive mediator of some pathways of TLR-mediated gene expression, the opposite hypothesis was also considered. Herein, we observed that flagellin stimulation of epithelial cells indeed induced rapid (