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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Toll-like receptor adaptor molecule 2

TIRP is a Toll/interleukin-1 receptor (IL1R; MIM 147810) (TIR) domain-containing adaptor protein involved in Toll receptor signaling (see TLR4; MIM 603030).[supplied by OMIM, Apr 2004] (from NCBI)
Top mentioned proteins: MyD88, TLR4, V1a, TLR3, CAN
Papers using TRAM antibodies
Mitogenic modulation of Ca2+ -activated K+ channels in proliferating A7r5 vascular smooth muscle cells.
Asanuma Masato, In PLoS ONE, 2005
... 1-[(2-Chlorophenyl)diphenylmethyl]-1H-pyrazole (TRAM-34) was purchased from Tocris Biosciences (Ellisville, MO, USA) ...
Cutting Edge: NF-kappaB-activating kinase-associated protein 1 participates in TLR3/Toll-IL-1 homology domain-containing adapter molecule-1-mediated IFN regulatory factor 3 activation
Li Kui, In PLoS ONE, 2004
... Antibodies against Flag, Myc, HA, and β-actin were purchased from Sigma; rabbit anti-TRIF and anti-TRAF3 antibodies were from Cell Signaling Technology (Danvers, MA) ...
Papers on TRAM
Primary role for TLR-driven TNF rather than cytosolic immune detection in restricting Coxiella burnetii phase II replication within mouse macrophages.
Shin et al., Ribeirão Preto, Brazil. In Infect Immun, Feb 2016
Furthermore, the TLR signaling adaptors MyD88 and Trif are required for cytokine responses and restricting bacterial replication.
Single TRAM domain RNA-binding proteins in Archaea: functional insight from Ctr3 from the Antarctic methanogen Methanococcoides burtonii.
Cavicchioli et al., Sydney, Australia. In Environ Microbiol, Feb 2016
UNASSIGNED: TRAM domain proteins present in Archaea and Bacteria have a β-barrel shape with anti-parallel β-sheets that form a nucleic acid binding surface; a structure also present in cold shock proteins (Csps).
1-[4-Fluoro-2-(2-nitrovinyl)phenyl]pyrrolidine Suppresses Toll-like Receptor 4 Dimerization Induced by Lipopolysaccharide.
Youn et al., Asan, South Korea. In J Immunoassay Immunochem, Feb 2016
UNASSIGNED: Toll-like receptor 4 (TLR4) recognizes LPS and triggers the activation of the myeloid differential factor 88 (MyD88)- and toll-interleukin-1 receptor domain-containing adapter, inducing interferon-β (TRIF)-dependent major downstream signaling pathways.
Adiponectin Receptor Agonist, AdipoRon, Causes Vasorelaxation Predominantly Via a Direct Smooth Muscle Action.
Hill et al., Columbia, United States. In Microcirculation, Feb 2016
Inhibition of endothelium-dependent relaxation with combinations of L-NAME/indomethacin/apamin/TRAM-34 only slightly reduced adipoRon-mediated vasorelaxation in cerebral and coronary arteries.
Endothelium Dependent Hyperpolarization-Type Relaxation Compensates for Attenuated Nitric Oxide-Mediated Responses in Subcutaneous Arteries of Diabetic Patients.
Ghulam Rasool et al., Kota Baharu, Malaysia. In Nitric Oxide, Feb 2016
Acetylcholine-induced nitric oxide (NO)-mediated relaxations [in the presence of an inhibitor of cyclooxygenases (COX; indomethacin) and small and intermediate conductance calcium-activated potassium channel blockers (UCL1684 and TRAM 34, respectively)] were attenuated in arteries from diabetics compared to controls (P < 0.001).
The immunobiology of Campylobacter jejuni: Innate immunity and autoimmune diseases.
Phongsisay, Fukuoka, Japan. In Immunobiology, Jan 2016
Furthermore, C. jejuni targets MyD88, NLRP3 inflammasome, TIR-domain-containing adapter-inducing interferon-β (TRIF), sialic acid-binding immunoglobulin-like lectins (Siglecs), macrophage galactose-type lectin (MGL), and immunoglobulin-like receptors (TREM2, LMIR5/CD300b).
Invariant chain is a new chaperone for TLR7 in B cells.
Manoury et al., Boston, United States. In Mol Immunol, Dec 2015
Upon stimulation, they relocate to the endo-lysosomal compartment, allowing the recruitment of the adaptor molecules, MyD88 or TRIF.
A tale of two domains - a structural perspective of the pseudokinase, MLKL.
Murphy et al., Australia. In Febs J, Nov 2015
We review the current understanding and gaps in knowledge relating to how MLKL can be activated by receptor interacting protein kinase (RIPK)3 downstream of tumour necrosis factor receptor 1:RIPK1, Toll like receptor-3:TRIF and viral DNA: DAI (DNA-dependent activator of interferon regulatory factors)/ZBF1.
Crosstalk between Gut Microbiota and Dietary Lipids Aggravates WAT Inflammation through TLR Signaling.
Bäckhed et al., Göteborg, Sweden. In Cell Metab, Nov 2015
Trif(-/-) and Myd88(-/-) mice are protected against lard-induced WAT inflammation and impaired insulin sensitivity.
CD47 blockade triggers T cell-mediated destruction of immunogenic tumors.
Xu et al., Beijing, China. In Nat Med, Oct 2015
In addition, the antitumor effects of CD47 blockade required expression of the cytosolic DNA sensor STING, but neither MyD88 nor TRIF, in CD11c+ cells, suggesting that cytosolic sensing of DNA from tumor cells is enhanced by anti-CD47 treatment, further bridging the innate and adaptive responses.
Phosphorylation of innate immune adaptor proteins MAVS, STING, and TRIF induces IRF3 activation.
Chen et al., Dallas, United States. In Science, Apr 2015
We further show that TRIF, an adaptor protein in Toll-like receptor signaling, activates IRF3 through a similar phosphorylation-dependent mechanism.
TLR3 and its roles in the pathogenesis of type 2 diabetes.
Kennedy et al., Zābol, Iran. In Cell Mol Biol (noisy-le-grand), 2014
TLR3 has been identified as an intracellular ligand and subsequently activates signaling molecules via the TRIF pathway.
TLR5 expression in the small intestine depends on the adaptors MyD88 and TRIF, but is independent of the enteric microbiota.
Reinhardt et al., Mainz, Germany. In Gut Microbes, 2014
In this study, MyD88 and TRIF expression in the small intestine were affected by gut microbiota.
Programmed necrosis in the cross talk of cell death and inflammation.
Moriwaki et al., Worcester, United States. In Annu Rev Immunol, 2014
RIPK3 partners with its upstream adaptors RIPK1, TRIF, or DAI to signal for necroptosis in response to death receptor or Toll-like receptor stimulation, pathogen infection, or sterile cell injury.
RIPK1 blocks early postnatal lethality mediated by caspase-8 and RIPK3.
Green et al., Memphis, United States. In Cell, 2014
Disruption of TLR (TRIF) or type I interferon (IFNAR) signaling delayed lethality in ripk1(-/-)tnfr1(-/-) mice.
TRIF licenses caspase-11-dependent NLRP3 inflammasome activation by gram-negative bacteria.
Fitzgerald et al., Worcester, United States. In Cell, 2012
Caspase-11 activation via the TLR4-TRIF-IFNbeta pathway synergizes with the NLRP3 pathway to coordinate caspase-1-dependent IL-1beta and IL-18 secretion and also leads to caspase-1-independent cell death.
Bacterial RNA mediates activation of caspase-1 and IL-1β release independently of TLRs 3, 7, 9 and TRIF but is dependent on UNC93B.
Dalpke et al., Heidelberg, Germany. In J Immunol, 2012
Secretion of interleukin (IL)-1beta upon bacterial RNA stimulation is independent of TRIF.
Toll/interleukin-1 receptor domain-containing adapter inducing interferon-β mediates microglial phagocytosis of degenerating axons.
Venkatesan et al., Baltimore, United States. In J Neurosci, 2012
This study provided the evidence that TRIF-mediated signaling plays an unexpected role in axonal debris clearance by microglia, thereby facilitating a more permissive environment for axonal outgrowth.
The Asp299Gly polymorphism alters TLR4 signaling by interfering with recruitment of MyD88 and TRIF.
Medvedev et al., Baltimore, United States. In J Immunol, 2012
the D299G polymorphism compromises recruitment of MyD88 and TRIF to TLR4 without affecting TLR4 expression, TLR4-MD2 interaction, or LPS binding, suggesting that it interferes with TLR4 dimerization
Both TLR2 and TRIF contribute to interferon-β production during Listeria infection.
Cossart et al., Paris, France. In Plos One, 2011
TLR2 and TRIF are two critical components leading to the induction of the IFN-beta gene during Listeria infection.
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