Signaling to NF-kappaB by Toll-like receptors.

By Taro Kawai, Shizuo Akira. Trends in Molecular Medicine, 2007

967 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/ddd71eca518e4da9823d4aeb89a570b9490205ca

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Citations in the corpus

• The NLRP3 inflammasome protects against loss of epithelial integrity and mortality during experimental colitis (2010, unknown): “TLRs are membrane-bound receptors that detect pathogen-associated molecular patterns (PAMPs) in the extracellular milieu (Kawai and Akira, 2007).”
• Persistent inflammation and immunosuppression: A common syndrome and new horizon for surgical intensive care (2012, background): “The end results were similar, that is, the activation and overexpression of early response genes, driven in large part through nuclear factor JB (NF-kB) activation.(31) There have been nearly 150 clinical trials of biologic responsemodifiers,most testing agents that attempt to block this early proin”
• NF-κB signaling in inflammation (2017, unknown): “34, 35 Activated TBK1 and IKK ε then phosphorylate the transcription factor IRF3 and, thereby, induce IRF3 dimerization, leading to transcriptional induction of type I IFNs, IFN-α and IFN-β .”
• Para-inflammation in the aging retina. (2009, background): “So far, 13 different TLRs have been identified in mouse and analysis of the human genome database has revealed the existence of 11 TLR homologues in human (Kawai and Akira, 2007b; Rock et al., 1998).”
• Inflammation and Pregnancy (2006, background): “The TLR signaling pathway ultimately leads to changes in gene transcription through the action of NF- B.(39) Major targets of NF- B are the genes that encode proinflammatory cytokines, including TNF-a and IL-1-b.”
• Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses (2009, background): “One concern is whether a TLR4 agonist may mimic the effects of LPS and induce endotoxic shock (177).”
• Toll-like receptors in antiviral innate immunity (2013, background): “As a result, NF-κB is liberated and migrates into the nucleus whereby it binds and activates target gene promoters such as those of IFN-β and numerous cytokines [31,32].”
• Pseudomonas aeruginosa: pathogenesis, virulence factors, antibiotic resistance, interaction with host, technology advances and emerging therapeutics (2022, background): “pathogen-associated molecular patterns (PAMPs), TLRs activate NF-κB and AP-1 to mediate inflammatory response signal pathways.(270) Correspondingly, TLRs are capable of recognizing different pathogen-associated molecular patterns found in P.”