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SLAMF1 is required for TLR4-mediated TRAM-TRIF-dependent signaling in human macrophages.
These data indicate a novel role of the TLR3-TICAM-1 pathway in controlling miR-21 levels in extracellular vesicles.
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.
The down regulation of TRIF, TLR3, and mitochondrial antiviral signaling protein (MAVS) expressions in chronic hepatitis C correlates with the disease severity and the outcome of hepatitis C virus infection
TRIM56 may act as a tumor suppressor in multiple myeloma through activation of TLR3/TRIF signaling pathway.
Data suggest that endosomal localization of TICAM2 is essential for TLR4-mediated type I interferon-inducing signaling from endosomes; TICAM2 acts as scaffold protein and activates TICAM1; N-terminal myristoylation allows TICAM2 to anchor to endosomal membrane. (TICAM2 = toll like receptor adaptor molecule-2; TICAM1 = toll like receptor adaptor molecule-1; TLR4 = toll-like receptor 4) [REVIEW]
Data suggest that pro-death signals through TIR-domain-containing adapter-inducing interferon-beta (TRIF) are regulated by autophagy and propose that pro-apoptotic signalling through TRIF/RIPK1/caspase-8 occurs in fibrillary platforms.
Therefore, Seneca Valley virus suppressed antiviral interferon production to escape host antiviral innate immune responses by cleaving host adaptor molecules MAVS, TRIF, and TANK by its 3C protease.
TRIF gene may contribute to susceptibility of T2DM.
The NF-kappaB activated by dsRNA appears not to be the canonical p65/p50 heterodimers.
We confirmed associations with papillary thyroid cancer and SNPs in FOXE1/HEMGN, SERPINA5 (rs2069974), FTO (rs8047395), EVPL (rs2071194), TICAM1 (rs8120) and SCARB1 (rs11057820) genes. We found associations with SNPs in FOXE1, SERPINA5, FTO, TICAM1 and HSPA6 and and follicular thyroid cancer
IL-12p70 production requires uptake of Streptococcus pneumoniae as well as the presence of the adaptor molecule TRIF.
TIRF high-content imaging system simultaneously showed the expression pattern of EGFRs and EC50 value for CPT-induced apoptosis and necrosis in MCF-7, SK-BR-3 and JIMT-1 cancer cell line
involved in signaling that moderates the expression of heme oxygenase1 and il-8 after keratinocytes exposure to dinitrochlorobenzene
Using bone marrow derived macrophages from knockout mice we demonstrate that hBD3 suppresses the polyI:C-induced TLR3 response mediated by TICAM1 (TRIF), while exacerbating the cytoplasmic response through MDA5 (IFIH1) and MAVS (IPS1/CARDIF).
signaling through TRIF is important for the inflammatory response of AngII-induced abdominal aortic aneurysm formation
Data show that toll-like receptor 3/TRIF protein signalling regulates cytokines IL-32 and IFN-beta secretion by activation of receptor-interacting protein-1 (RIP-1) and tumour necrosis factor receptor-associated factor 6 (TRAF6) in cornea epithelial cells.
WDFY1 mediates TLR3/TLR4 signaling by recruiting TRIF.
In mice with nonfunctional TRIF (Trif(mut) mice), Ang II-induced hypertension and cardiac hypertrophy were abrogated, and proinflammatory gene expression in heart and kidneys was unchanged or decreased. These results indicate that Ang II induces activation of a proinflammatory innate immune response, causing hypertension and cardiac hypertrophy, which require functional adaptor protein TRIF-mediated pathways.
TRIF promotes angiotensin II-induced cross-talk between fibroblasts and macrophages in atrial fibrosis.
The TRIF pathway plays an important role in protecting a microenvironment surrounding motor neurons by eliminating aberrantly activated astrocytes.
These data suggest that TLR3 signaling controls the onset and severity of acute pancreatitis.
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.
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.
STING-mediated innate immune responses and dendritic cell maturation do not require TICAM-1 in myeloid lineage immune cells.
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.
The TLR3/TICAM-1 pathway inhibits polyposis through suppression of c-Myc expression and supports long survival in Apc (Min/+) mice.
Versican is produced by Trif- and type I interferon-dependent signaling in macrophages and contributes to fine control of innate immunity in lungs
TRIF contributes to murine host defense during the initial response to leptospiral infection
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.
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.
TRIF and STING interacted directly, through their carboxy-terminal domains, to promote STING dimerization, intermembrane translocation, and signaling.
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.
These results suggested the importance of TRIF in TLR2 mediated foam cell formation via inflammatory mediators, including MCP-1.
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
The authors demonstrate that, in addition to MyD88, Yersinia pseudotuberculosis inhibits TRIF signaling through the type III secretion system effector YopJ.
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).
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.
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
Inhibition of the Toll/interleukin-1 receptor (TIR) domain-containing adapter-inducing interferon-beta signaling reduced permeability changes and apoptosis in endothelial cells exposed to lipopolysaccharide.
3D-models of rohu TLR3-TIR and zebrafish TRIF
The role of zebrafish (Danio rerio) TICAM1 in activating NF-kappaB and zebrafish type I IFN was described.
study focuses on the functional characterization of zebrafish TRIF; results show that the full length cDNA of zebrafish TRIF encodes a protein of 556 amino acids; TRIF is able to induce the IFN promoter as well as activate NF-kappaB response promoter
This gene encodes an adaptor protein containing a Toll/interleukin-1 receptor (TIR) homology domain, which is an intracellular signaling domain that mediates protein-protein interactions between the Toll-like receptors (TLRs) and signal-transduction components. This protein is involved in native immunity against invading pathogens. It specifically interacts with toll-like receptor 3, but not with other TLRs, and this association mediates dsRNA induction of interferon-beta through activation of nuclear factor kappa-B, during an antiviral immune response.
TIR domain containing adaptor inducing interferon-beta
, TIR domain-containing adapter molecule 1
, TIR domain-containing adapter protein inducing IFN-beta
, proline-rich, vinculin and TIR domain-containing protein B
, putative NF-kappa-B-activating protein 502H
, toll-interleukin-1 receptor domain-containing adapter protein inducing interferon beta
, toll-interleukin I receptor domain containing adaptor molecule 1
, toll-like receptor adaptor molecule 1
, TIR domain-containing adapter molecule 1-like
, TIR domain-containing adaptor inducing interferon-beta
, toll-interleukin 1 receptor domain-containing adapter protein inducing interferon-beta
, TIR-domain containing adaptor inducing IFN-beta