Signaling to NF-?B by Toll-like receptors

By Taro Kawai, Shizuo Akira. 2007

2,141 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/35c59e382bfec4aee40c11e80db611348dd8262e

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Citations in the corpus

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).”
microRNA regulation of inflammatory responses. (2012, background): “Both pathways activate NF-κB, a central mediator of the innate immune response leading to inflammation (27).”
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).”
ZBP1 and TAK1: Master Regulators of NLRP3 Inflammasome/Pyroptosis, Apoptosis, and Necroptosis (PAN-optosis) (2019, background): “However, membrane-bound PRRs, such as Toll-like receptors (TLRs) and cytokine receptors such as tumor necrosis factor (TNF) receptor 1 (TNFR1), often show a bias toward induction of the inflammatory immune response through the NF-κB and MAPK pathways, despite having all the principal components requ”
Astrocyte crosstalk in CNS inflammation (2020, background): “…as tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-17 (Qian et al., 2007), reactive oxygen species (ROS) (Chandel et al., 2000), phagocytosed myelin (Ponath et al., 2017), Toll-like receptor (TLR) engagement (Kawai and Akira, 2007) and other factors associated with CNS inflammation (Fig.”