LPS/TLR4 signal transduction pathway.
By Yong-Chen Lu, W. Yeh, P. Ohashi. Cytokine, 2008
3,116 citations recorded by the source corpus.
Subfields: Cancer Research, Immunology, Microbiology
View Paper: https://www.semanticscholar.org/paper/fefb1b4493d8c0d85e00bc8e4474c110da80a68a
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
- Maren Keller
- J. Mazuch
- U. Abraham
- G. Eom
- H. Volk
- A. Sarkar
- A. Kramer
- S. Dutra
Citations in the corpus
- Gut Microbiota and Immune System Interactions (2020, background): “The activation of TLR4 in pancreatic islets was shown to increase proinflammatory cytokine production in macrophages and beta-cells, resulting in decreased function and viability of beta-cells [103].”
- NF-κB signaling in inflammation (2017, neutral): “24,25 Upon activation, TAK1 activates the downstream kinase IKK, which in turn phosphorylate the NF-κ B inhibitor I κ B α , leading to ubiquitin-dependent I κ B α degradation and NF-κ B activation.”
- Gut microbiota, intestinal permeability, and systemic inflammation: a narrative review (2023, background): “This binding could depend on a structural similarity between dietary SFA and the Lipid A of LPS; indeed, SFA’ pro-inflammatory potency varies according to chain lengths, with lauric acid showing the highest pro-inflammatory activity and the myristic acid and the stearic acid the lowest [24].”
- A circadian clock in macrophages controls inflammatory immune responses (2009, background): “This pathway is complex and includes transcriptional but also posttranscriptional, translational, and posttranslational events (25).”