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Human Toll-Like Receptor Adaptor Molecule 2 (TICAM2) interaction partners

1. Data suggest that endosomal localization of TICAM2 is essential for TLR4 (show TLR4 Antibodies)-mediated type I interferon (show IFNA Antibodies)-inducing signaling from endosomes; TICAM2 acts as scaffold protein (show HOMER1 Antibodies) and activates TICAM1 (show TICAM1 Antibodies); N-terminal myristoylation allows TICAM2 to anchor to endosomal membrane. (TICAM2 = toll like receptor adaptor molecule-2; TICAM1 (show TICAM1 Antibodies) = toll like receptor adaptor molecule-1 (show TICAM1 Antibodies); TLR4 (show TLR4 Antibodies) = toll-like receptor 4 (show TLR4 Antibodies)) [REVIEW]

2. Data show that Toll (show TLR4 Antibodies)/IL-1R domain-containing adaptor molecule (TICAM)-2 possesses two conserved acidic amino acids, D91 and E92, which regulate TICAM-2 self-activation and signaling.

3. Findings were SNPs in TICAM2 (P = 3.6 x 10(-6)) and IL1B (show IL1B Antibodies) (P = 4.3 x 10(-5)) associated with TB.

4. TRAM (show TRAM1 Antibodies) plays a role in TLR7 (show TLR7 Antibodies) signaling through a novel signaling axis towards the activation of anti-viral immunity.

5. TRAM acts as a sorting adaptor not only for TLR4, but also for TLR2, to facilitate signaling to IRF7 at the endosome, which explains how TLR2 is capable of causing type I IFN induction.

6. A putative TRAF6 (show TRAF6 Antibodies)-binding motif in TRAM (show TRAM1 Antibodies) may mediate a new TRAM (show TRAM1 Antibodies) function in TLR4 (show TLR4 Antibodies) signaling in regulating inflammatory responses, distinct from its bridging TLR4 (show TLR4 Antibodies) and TRIF (show TRIM69 Antibodies). A TRAM (show TRAM1 Antibodies) E183A mutation abolished this.

7. results suggest TLR adaptor molecules knockdown, such as MyD88 (show MYD88 Antibodies) or TRAM (show TRAM1 Antibodies), can decrease IL-6 (show IL6 Antibodies) and IL-8 (show IL8 Antibodies) mRNA and increase CXCL12 (show CXCL12 Antibodies) mRNA expression in HGF (show HGF Antibodies) and HPDLF.

8. The homotypic interaction between TICAM-2 TIR is indispensable to present a scaffold for recruiting the monomeric moiety of the TICAM-1 (show TICAM1 Antibodies) TIR dimer.

9. induction of both IL-6 (show IL6 Antibodies) and IL-8 (show IL8 Antibodies) is associated with elevated TIRAP (show TIRAP Antibodies) and reduced TRAM (show TRAM1 Antibodies) mRNA expression

10. Data indicate that MyD88 works together with the IL-1/IL-18 receptors, can interact with two distinct sorting adaptors, TRAM and Mal, in a conserved manner.

Mouse (Murine) Toll-Like Receptor Adaptor Molecule 2 (TICAM2) interaction partners

1. Using ovalbumin (show OVA Antibodies) as model antigen, the authors showed that exposure of dendritic cells to hyperosmolarity strongly inhibits activation of antigen-specific T cells despite enhancement of antigen uptake, processing and presentation. They identified TRIF (show RNF138 Antibodies) as key mediator of this phenomenon.

2. the present study indicated that MyD88 (show MYD88 Antibodies) and TRIF (show RNF138 Antibodies) blockades serve notable and equivalent roles in protecting cardiac deterioration from severe sepsis by attenuating cytokine release, reducing neutrophil infiltration and alleviating apoptosis.

3. lipopolysaccharide (LPS (show TLR4 Antibodies)) application induces proliferation of dormant hematopoietic stem cells (HSC (show FUT1 Antibodies)) and impairs HSC (show FUT1 Antibodies) self-renewal via TLR4 (show TLR4 Antibodies)-TRIF (show RNF138 Antibodies)-ROS (show ROS1 Antibodies)-p38 (show CRK Antibodies) signaling.

4. These results indicate a critical role for Ticam2 in SARS (show SARS Antibodies)-CoV disease, and highlight the importance of host genetic variation in disease responses.

5. Distinct mechanisms downstream of TLR4 (show TLR4 Antibodies) signaling mediate myelosuppression and hematopoietic stem cell exhaustion during sepsis through unique effects of MyD88 (show MYD88 Antibodies) and TRIF (show RNF138 Antibodies).

6. these data show that both Myd88 (show MYD88 Antibodies) and TRIF (show RNF138 Antibodies) are necessary for Th17 differentiation in the lungs in response to immunization with lipopolysaccharide

7. these studies reveal an additional regulatory function of TRIM8 (show TRIM8 Antibodies) in innate immune responses: TRIM8 (show TRIM8 Antibodies) catalyzes polyubiquitination of TRIF (show RNF138 Antibodies), resulting in disruption of TRIF (show RNF138 Antibodies)-TBK1 (show TBK1 Antibodies) interaction

8. Stimulation of the TLR4 (show TLR4 Antibodies)-TRIF (show RNF138 Antibodies) pathway can protect against the development of allergic airway disease and that a TRIF (show RNF138 Antibodies)-dependent adjuvant effect on CD4 (show CD4 Antibodies)(+) ICOS (show ICOS Antibodies)(+) T-cell responses may be a contributing mechanism.

9. Monophosphoryl lipid A stimulation of a TLR4 (show TLR4 Antibodies)-TRIF (show RNF138 Antibodies)-PI3K-Akt (show AKT1 Antibodies) pathway prevents lipopolysaccharide-induced ERK (show EPHB2 Antibodies) activation in the medullar thick ascending limb.

10. study reporst a key role for TNF (show TNF Antibodies)/TNFR1 (show TNFRSF1A Antibodies) in Yersinia-induced cell death of murine macrophages, which occurs despite the blockade of NF-kappaB (show NFKB1 Antibodies) and MAPK (show MAPK1 Antibodies) signaling imposed by Yersinia on infected cells