TRAM couples endocytosis of Toll-like receptor 4 to the induction of interferon-β

By Jonathan C. Kagan, Tian Su, T. Horng, A. Chow, Shizuo Akira, R. Medzhitov. Nature Immunology, 2008

1,119 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/57e5a243bf719d32c6e3226d14081226752c3bc5

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In Immunology

Citations in the corpus

Co-operation of TLR4 and raft proteins in LPS-induced pro-inflammatory signaling (2014, background): “The endocytosis of TLR4 is supposed to follow MyD88-dependent signaling originating from the plasma membrane [27, 105, 106] and the switch from the plasma membrane MyD88-based to the TRIF-dependent endosomal signaling of TLR4 could be controlled by phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] t”
The interleukin‐1 receptor/Toll‐like receptor superfamily: 10 years of progress (2008, background): “TLR4 has recently been shown to signal from two locations (58).”
CD36 ligands promote sterile inflammation through assembly of a Toll-like receptor 4 and 6 heterodimer (2009, background): “We therefore tested whether fibrillar β-amyloid peptide (1-42) (Aβ1-42) could activate TLR4-TLR6 signaling via CD36.”
Innate Immune Pattern Recognition: A Cell Biological Perspective (2015, neutral): “The sorting adaptor TRAM contains a bipartate N-terminal localization signal containing a myristate group and a polybasic motif that control trafficking between the plasma membrane and endosomes (23, 150).”
Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses (2009, neutral): “Thus, molecular signaling mechanisms within the TRIF-dependent pathway illustrate how selective binding of different molecules, i.e., either TRAF3 or TRAF6, results in recruitment and downstream activation of TBK1-IRF versus TAK1-IKK-NF- B, respectively (Fig.”
Pathogen Recognition by the Innate Immune System (2011, background): “This complex initiates the TRIF-dependent signaling required for IRF3 activation, which induces type I interferon and this signaling pathway activates second-phase of NFκB and MAPK activation for the induction of inflammatory cytokines [26].”
NF-κB Signaling in Macrophages: Dynamics, Crosstalk, and Signal Integration (2019, background): “TLR4 signaling through the adaptor molecule MyD88 leads to the activation of NF-κB, mitogenactivated protein kinase (MAPK), and IRF5 pathways (30), while subsequent endosomal TLR4 signaling through TIR-domaincontaining adaptor protein inducing interferon-β (TRIF) leads to the activation of IRF3, and”
TLR4 and CD14 trafficking and its influence on LPS-induced pro-inflammatory signaling (2020, background): “The TLR4 endocytosis depends on dynamin, a GTPase responsible for pinching off of clathrin-coated buds, some macro- and micropinosomes, and phagosomes [157, 158] inhibition of dynamin with dynasore prevented LPS-induced internalization of TLR4 in several cell types, including macrophages [40, 141, 1”
TRIF Licenses Caspase-11-Dependent NLRP3 Inflammasome Activation by Gram-Negative Bacteria (2012, positive): “TRIF is recruited to TLR4 via TRAM or directly to the TIR domain of TLR3 (Kagan et al., 2008; Yamamoto et al., 2003).”