Phosphoinositide-mediated adaptor recruitment controls Toll-like receptor signaling.

By Jonathan C. Kagan, R. Medzhitov. Cell, 2006

892 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/3264440f38660f6de4cbbc602973e40326a6f5b1

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In Immunology

1. Shizuo Akira
2. R. Medzhitov
3. Taro Kawai
4. S. Ghosh
5. Jonathan C. Kagan
6. M. Hayden
7. G. Barton
8. A. West

Citations in the corpus

• CD14 controls the LPS-induced endocytosis of Toll-like Receptor 4 (2011, background): “This pathway is mediated by a pair of sorting and signaling adaptor proteins called TIRAP and MyD88, respectively (Kagan and Medzhitov, 2006).”
• NF-κB and the immune response (2006, background): “Recent reports suggest that the requirement for these intermediatory adapters is related to localization of the TLRs to certain domains in the plasma membrane (Kagan and Medzhitov, 2006; Rowe et al., 2006).”
• Toll-Like Receptor Signaling Pathways (2014, background): “Thus, TIRAP associates with both cell surface and endosomal TLRs by binding to different lipids (38).”
• Complement System Part II: Role in Immunity (2015, background): “In turn, CR3 can regulate TLR2 signalization by recruiting TIRAP and facilitating the recruitment of MyD88 signaling adaptor to initiate TLR signaling (123).”
• Innate Immune Pattern Recognition: A Cell Biological Perspective (2015, neutral): “Following ligand binding, the receptor engages TIRAP/MyD88 to initiate signaling from the cell surface and then undergoes endocytosis and engages TRAM/TRIF-dependent signaling from endosomes (22, 23).”
• Seeded Bayesian Networks: Constructing genetic networks from microarray data (2008, background): “Detection of pathogen molecules by these receptors results in the recruitment of various adaptor proteins and the activation of downstream signal transduction cascades [9,10].”
• TLR4 and CD14 trafficking and its influence on LPS-induced pro-inflammatory signaling (2020, background): “7 cells, the LPS-induced activation of NF-κB was lower than in their wild type counterparts suggesting a down-regulation of the MyD88-dependent signaling due to insufficient PI(4,5)P2 generation in the plasma membrane [73, 152].”
• A cell biological view of Toll-like receptor function: regulation through compartmentalization (2009, methodology): “This model was challenged by several recent articles showing that TIRAP and TRAM are found on intracellular membranes before the initiation of signal transductio”
• TRAM couples endocytosis of Toll-like receptor 4 to the induction of interferon-β (2008, background): “Unlike the signaling adaptor MyD88, TIRAP functions as a sorting adaptor that recruits MyD88 to TLR4 through its ability to interact with phosphatidylinositol-4,5-bisphosphate (PtdIns(4,5)P 2”
• Co-operation of TLR4 and raft proteins in LPS-induced pro-inflammatory signaling (2014, background): “The drop of PI(4,5)P2 level in the membrane of endosomes was proposed to facilitate the disassembly of the TIRAP/MyD88 signaling complex and association of TRAM/TRIF adaptors [27, 107].”