| ZCCHC3 modulates TLR3-mediated signaling by promoting recruitment of TRIF to TLR3. | ZCCHC3 modulates TLR3-mediated signaling by promoting recruitment of TRIF to TLR3.
Zang R, Lian H, Zhong X, Yang Q, Shu HB., Free PMC Article | 08/14/2021 |
| ferroptosis orchestrates neutrophil recruitment to injured myocardium by promoting adhesion of neutrophils to coronary vascular endothelial cells through a TLR4/TRIF/type I IFN signaling pathway. | Ferroptotic cell death and TLR4/Trif signaling initiate neutrophil recruitment after heart transplantation.
Li W, Feng G, Gauthier JM, Lokshina I, Higashikubo R, Evans S, Liu X, Hassan A, Tanaka S, Cicka M, Hsiao HM, Ruiz-Perez D, Bredemeyer A, Gross RW, Mann DL, Tyurina YY, Gelman AE, Kagan VE, Linkermann A, Lavine KJ, Kreisel D., Free PMC Article | 04/18/2020 |
| TRIF K27-linked polyubiquitination and deubiquitination as a critical regulatory mechanism of TLR3/4-mediated innate immune responses. | Regulation of TRIF-mediated innate immune response by K27-linked polyubiquitination and deubiquitination.
Wu X, Lei C, Xia T, Zhong X, Yang Q, Shu HB., Free PMC Article | 12/28/2019 |
| The TRIF pathway plays an important role in protecting a microenvironment surrounding motor neurons by eliminating aberrantly activated astrocytes. | Innate immune adaptor TRIF deficiency accelerates disease progression of ALS mice with accumulation of aberrantly activated astrocytes.
Komine O, Yamashita H, Fujimori-Tonou N, Koike M, Jin S, Moriwaki Y, Endo F, Watanabe S, Uematsu S, Akira S, Uchiyama Y, Takahashi R, Misawa H, Yamanaka K., Free PMC Article | 10/19/2019 |
| These data suggest that TLR3 signaling controls the onset and severity of acute pancreatitis. | Loss of TLR3 and its downstream signaling accelerates acinar cell damage in the acute phase of pancreatitis.
Regel I, Raulefs S, Benitz S, Mihaljevic C, Rieder S, Leinenkugel G, Steiger K, Schlitter AM, Esposito I, Mayerle J, Kong B, Kleeff J, Michalski CW. | 04/27/2019 |
| Together, our findings demonstrate that TRIF signaling is required for caspase-11-dependent immune responses and lethality in endotoxemia and sepsis, and provide novel mechanistic insights into how LPS induces caspase-11 activation during bacterial infection. | TRIF signaling is required for caspase-11-dependent immune responses and lethality in sepsis.
Tang Y, Zhang R, Xue Q, Meng R, Wang X, Yang Y, Xie L, Xiao X, Billiar TR, Lu B., Free PMC Article | 02/9/2019 |
| Findings confirm that signalling through MyD88 is the primary driver for Lipopolysaccharide-dependent NF-kappaB translocation to the nucleus. The pattern of NF-kappaB dynamics in TRIF-deficient cells does not, however, directly reflect the kinetics of TNFalpha promoter activation, supporting the concept that TRIF-dependent signalling plays an important role in the transcription of this cytokine. | Lipopolysaccharide-induced NF-κB nuclear translocation is primarily dependent on MyD88, but TNFα expression requires TRIF and MyD88.
Sakai J, Cammarota E, Wright JA, Cicuta P, Gottschalk RA, Li N, Fraser IDC, Bryant CE., Free PMC Article | 12/22/2018 |
| STING-mediated innate immune responses and dendritic cell maturation do not require TICAM-1 in myeloid lineage immune cells. | TICAM-1 is dispensable in STING-mediated innate immune responses in myeloid immune cells.
Takashima K, Oshiumi H, Matsumoto M, Seya T. | 10/13/2018 |
| Mice with myeloid cell specific TIR-domain-containing adapter-inducing interferon-beta (TRIF) knockout showed a trend towards accelerated onset of STZ-induced diabetes, while TRIF deficiency resulted in reduced IDO expression in vivo and in vitro. MyD88 signaling in myeloid cells is a critical pathogenic factor in autoimmune diabetes, which is antagonized by TRIF-dependent responses. | Differential role of MyD88 and TRIF signaling in myeloid cells in the pathogenesis of autoimmune diabetes.
Androulidaki A, Wachsmuth L, Polykratis A, Pasparakis M., Free PMC Article | 07/14/2018 |
| Findings suggest that Toll/IL-1R domain-containing adapter-inducing IFN-beta may be involved in the epileptogenesis of temporal lobe epilepsy, which would make it a potential therapeutic target for the treatment of epilepsy. | TRIF contributes to epileptogenesis in temporal lobe epilepsy during TLR4 activation.
Wang FX, Yang XL, Ma YS, Wei YJ, Yang MH, Chen X, Chen B, He Q, Yang QW, Yang H, Liu SY. | 07/14/2018 |
| The TLR3/TICAM-1 pathway inhibits polyposis through suppression of c-Myc expression and supports long survival in Apc (Min/+) mice. | The TLR3/TICAM-1 signal constitutively controls spontaneous polyposis through suppression of c-Myc in Apc (Min/+) mice.
Ono J, Shime H, Takaki H, Takashima K, Funami K, Yoshida S, Takeda Y, Matsumoto M, Kasahara M, Seya T., Free PMC Article | 05/19/2018 |
| Versican is produced by Trif- and type I interferon-dependent signaling in macrophages and contributes to fine control of innate immunity in lungs | Versican is produced by Trif- and type I interferon-dependent signaling in macrophages and contributes to fine control of innate immunity in lungs.
Chang MY, Kang I, Gale M Jr, Manicone AM, Kinsella MG, Braun KR, Wigmosta T, Parks WC, Altemeier WA, Wight TN, Frevert CW., Free PMC Article | 12/9/2017 |
| TRIF contributes to murine host defense during the initial response to leptospiral infection | The adaptor molecule Trif contributes to murine host defense during Leptospiral infection.
Jayaraman PA, Devlin AA, Miller JC, Scholle F. | 12/2/2017 |
| work reveals that simulated microgravity promotes the apoptotic response through a combined modulation of the Uev1A/TICAM/TRAF/NF-kappaB-regulated apoptosis and the p53/PCNA- and ATM/ATR-Chk1/2-controlled DNA-damage response pathways. | Simulated Microgravity Promotes Cell Apoptosis Through Suppressing Uev1A/TICAM/TRAF/NF-κB-Regulated Anti-Apoptosis and p53/PCNA- and ATM/ATR-Chk1/2-Controlled DNA-Damage Response Pathways.
Zhao T, Tang X, Umeshappa CS, Ma H, Gao H, Deng Y, Freywald A, Xiang J. | 09/23/2017 |
| Results show that Monophosphoryl lipid A-induced neutrophil and monocyte recruitment, expansion of bone marrow progenitors and augmentation of neutrophil adhesion molecule expression are regulated by both the MyD88- and TRIF-dependent pathways. | The role of MyD88- and TRIF-dependent signaling in monophosphoryl lipid A-induced expansion and recruitment of innate immunocytes.
Hernandez A, Bohannon JK, Luan L, Fensterheim BA, Guo Y, Patil NK, McAdams C, Wang J, Sherwood ER., Free PMC Article | 09/9/2017 |
| TRIF and STING interacted directly, through their carboxy-terminal domains, to promote STING dimerization, intermembrane translocation, and signaling. | STING Requires the Adaptor TRIF to Trigger Innate Immune Responses to Microbial Infection.
Wang X, Majumdar T, Kessler P, Ozhegov E, Zhang Y, Chattopadhyay S, Barik S, Sen GC., Free PMC Article | 08/26/2017 |
| Upon stimulation with poly(I:C), malaria parasite-infected red blood cells (iRBCs), or vesicular stomatitis virus (VSV), FOSL1 "translocated" from the nucleus to the cytoplasm, where it inhibited the interactions between TNF receptor-associated factor 3 (TRAF3), TIR domain-containing adapter inducing IFN-beta (TRIF), and Tank-binding kinase 1 (TBK1) via impairing K63-linked polyubiquitination of TRAF3 and TRIF. | FOSL1 Inhibits Type I Interferon Responses to Malaria and Viral Infections by Blocking TBK1 and TRAF3/TRIF Interactions.
Cai B, Wu J, Yu X, Su XZ, Wang RF., Free PMC Article | 07/1/2017 |
| These results suggested the importance of TRIF in TLR2 mediated foam cell formation via inflammatory mediators, including MCP-1. | TRIF is a regulator of TLR2-induced foam cell formation.
Huang B, Park DW, Baek SH. | 04/15/2017 |
| DENV replication and IFNalpha/beta, TNF-alpha, IL-12 and IL-18 in infected cultures at 24h were found. All of these parameters were significantly decreased after TRIF, MYD88 or NF-kB inhibition | Role of the myeloid differentiation primary response (MYD88) and TIR-domain-containing adapter-inducing interferon-β (TRIF) pathways in dengue.
Duran A, Valero N, Mosquera J, Delgado L, Alvarez-Mon M, Torres M. | 02/18/2017 |
| The authors demonstrate that, in addition to MyD88, Yersinia pseudotuberculosis inhibits TRIF signaling through the type III secretion system effector YopJ. | A Single Bacterial Immune Evasion Strategy Dismantles Both MyD88 and TRIF Signaling Pathways Downstream of TLR4.
Rosadini CV, Zanoni I, Odendall C, Green ER, Paczosa MK, Philip NH, Brodsky IE, Mecsas J, Kagan JC., Free PMC Article | 10/8/2016 |
| Results show that toll/IL-1 domain-containing adaptor inducing IFN-beta (TRIF) is essential for Toll-like receptors TLR3- and TLR4-mediated innate immune responses in peritoneal mesothelial cells (PMCs). | Toll/IL-1 domain-containing adaptor inducing IFN-β (TRIF) mediates innate immune responses in murine peritoneal mesothelial cells through TLR3 and TLR4 stimulation.
Hwang EH, Kim TH, Oh SM, Lee KB, Yang SJ, Park JH., Free PMC Article | 09/17/2016 |
| Data show that annexin A2 (AnxA2) directly exerted negative regulation of inflammatory responses through Toll-like receptor 4 (TLR4)-initiated TRAM protein-TRIF protein pathway occurring on endosomes. | Annexin A2 binds to endosomes and negatively regulates TLR4-triggered inflammatory responses via the TRAM-TRIF pathway.
Zhang S, Yu M, Guo Q, Li R, Li G, Tan S, Li X, Wei Y, Wu M., Free PMC Article | 09/10/2016 |
| ProTalpha preconditioning-induced prevention of retinal ischemic damage is mediated by selective activation of the TIR-domain-containing adapter-inducing interferon-beta interferon regulatory factor 3 pathway downstream of toll-like receptor 4 in microglia | Prothymosin-alpha preconditioning activates TLR4-TRIF signaling to induce protection of ischemic retina.
Halder SK, Matsunaga H, Ishii KJ, Ueda H. | 08/27/2016 |
| signaling through TRIF is important for the inflammatory response of AngII-induced abdominal aortic aneurysm formation | TRIF adaptor signaling is important in abdominal aortic aneurysm formation.
Vorkapic E, Lundberg AM, Mäyränpää MI, Eriksson P, Wågsäter D. | 04/30/2016 |
| analysis of how MyD88 and TRIF affect TLR4 activation | Distinct single-cell signaling characteristics are conferred by the MyD88 and TRIF pathways during TLR4 activation.
Cheng Z, Taylor B, Ourthiague DR, Hoffmann A., Free PMC Article | 04/23/2016 |