PI3K and negative regulation of TLR signaling.
By T. Fukao, S. Koyasu. Trends in immunology, 2003
696 citations recorded by the source corpus.
Subfields: Cancer Research, Immunology
View Paper: https://www.semanticscholar.org/paper/fa8d7f105f2d4e118a3f746f72bba1a5e53576af
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cancer Research
In Immunology
Citations in the corpus
- The skin microbiome (2011, background): “The mechanism of this discrimination is not fully clear, but may involve the induction of immune tolerance; TLRs may be desensitized by prolonged exposure to commensal microorganisms, either through decreased TLR expression on the cell surface or by activation of the TLR pathway inhibitors interleuk”
- Macrophage Polarization States in the Tumor Microenvironment (2021, background): “NF-κB is a master regulator of M1 activation [41].”
- The multifunctional NS1 protein of influenza A viruses. (2008, background): “Indeed, PI3K activation has been implicated in many cellular functions that are also regulated by NS1, such as cytokine-downregulation in DCs, enhancement of mRNA translation and suppression of innate signalling pathways (Fukao & Koyasu, 2003; Platanias, 2005).”
- Akt Signaling Pathway in Macrophage Activation and M1/M2 Polarization (2017, background): “Activation of the PI3K/Akt pathway is critical in restricting proinflammatory and promoting anti-inflammatory responses in TLR-stimulated macrophages (18), and has been considered as a negative regulator of TLR and NF-kB signaling in macrophages (15, 16) (Fig.”
- Cutting Edge: TREM-2 Attenuates Macrophage Activation1 (2006, background): “Previous studies have demonstrated that PI3K can inhibit TLR activation through activation of the inhibitory apoptosis signalregulating kinase ASK (17), and DAP12 is known to activate PI3K (6).”
- Akt1 controls macrophage response to LPS by regulating microRNAs (2009, background): “Previous studies have shown that PI-3K and its downstream target Akt are activated by TLR4 signals and that they may function in a feedback loop that inhibits the response to both the primary and secondary exposure to TLR4 activators (Fukao and Koyasu, 2003).”