TLR9 signals after translocating from the ER to CpG DNA in the lysosome
By E. Latz, A. Schoenemeyer, A. Visintin, Katherine A. Fitzgerald, Brian G. Monks, C. Knetter, E. Lien, N. Nilsen, T. Espevik, D. Golenbock. Nature Immunology, 2004
1,500 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/a8f1cf14abd5a5dc6238bb15ef0f2b9d39d8a99a
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In Immunology
- Shizuo Akira
- Taro Kawai
- R. Medzhitov
- O. Takeuchi
- Satoshi Uematsu
- Jonathan C. Kagan
- K. Takeda
- Katherine A. Fitzgerald
In Molecular Biology
Citations in the corpus
- Innate immune recognition of viral infection (2006, background): “Unlike the other TLRs, which are expressed mainly on cell surfaces and recognize bacterial components, TLR7, TLR8 and TLR9 are located exclusively in endosomal compartment”
- Toll-like receptor signalling (2004, background): “For example, TLR9 has recently been shown to be expressed in the endoplasmic reticulum, and it is recruited to endosomal/lysosomal compartments after stimulation with CpG-containing DN”
- Maintenance of colonic homeostasis by distinctive apical TLR9 signalling in intestinal epithelial cells (2006, background): “Because of its endosomal localization in immune cell”
- Toll-like receptors in antiviral innate immunity (2013, background): “Like the other intracellular TLRs, TLR9 localizes within the endoplasmic reticulum, endosomes, and lysosomes [137].”
- Toll-like receptor signalling in the intestinal epithelium: how bacterial recognition shapes intestinal function (2010, background): “In immune cells, TLR9 interacts with CpG ODNs in endosome”
- Toll-like receptors on hematopoietic progenitor cells stimulate innate immune system replenishment. (2006, background): “…TLR expression to predict the efficiency of responsiveness to particular TLR ligands because many TLR are intracellular and coreceptor components could influence avidity of receptor-ligand interactions (Matsumoto et al., 2003, Latz et al., 2004, Takeuchi et al., 2001, and Takeuchi et al., 2002).”
- Toll-like receptor 9 mediates innate immune activation by the malaria pigment hemozoin (2005, background): “Once captured by phagocytes such as macrophages and DCs, HZ accumulates in the phagosome where TLR9 can be recruited from the endoplasmic reticulum via PI3 kinases (20, 21), indicating that TLR9 may recognize HZ in phagosome.”
- TRAM couples endocytosis of Toll-like receptor 4 to the induction of interferon-β (2008, background): “Studies have identified a notable aspect of TLR biology: a link between receptor localization, the type of transcriptional response induced and the class of microbe detecte”
- Therapeutic targeting of innate immunity with Toll-like receptor agonists and antagonists (2007, background): “TLR1, 2, 4, 5, 6 and 10 are expressed on the cell surface and migrate to phagosomes after activation, whereas TLR3, 7, 8 and 9 are expressed in intracellular compartments in nearly all cell types, principally in the endosomes and the endoplasmic reticulum, with the ligand-binding domains sampling th”
- Plasmacytoid dendritic cells: sensing nucleic acids in viral infection and autoimmune diseases (2008, background): “In the absence of PAMPs, TLR9 resides in the endoplasmic reticulum (ER) of resting pDCs, and only translocates to the endosomal compartment on exposure to TLR agonist”
- Silica crystals and aluminum salts mediate NALP-3 inflammasome activation via phagosomal destabilization (2008, background): “34 ), which signals from within endo-lysosomal compartment”