Aperçu des produits pour anti-TICAM2 (TICAM2) Anticorps

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

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

2. Data show that Toll (Montrer TLR4 Anticorps)/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 (Montrer IL1B Anticorps) (P = 4.3 x 10(-5)) associated with TB.

4. TRAM (Montrer TRAM1 Anticorps) plays a role in TLR7 (Montrer TLR7 Anticorps) 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 (Montrer TRAF6 Anticorps)-binding motif in TRAM (Montrer TRAM1 Anticorps) may mediate a new TRAM (Montrer TRAM1 Anticorps) function in TLR4 (Montrer TLR4 Anticorps) signaling in regulating inflammatory responses, distinct from its bridging TLR4 (Montrer TLR4 Anticorps) and TRIF (Montrer TRIM69 Anticorps). A TRAM (Montrer TRAM1 Anticorps) E183A mutation abolished this.

7. results suggest TLR adaptor molecules knockdown, such as MyD88 (Montrer MYD88 Anticorps) or TRAM (Montrer TRAM1 Anticorps), can decrease IL-6 (Montrer IL6 Anticorps) and IL-8 (Montrer IL8 Anticorps) mRNA and increase CXCL12 (Montrer CXCL12 Anticorps) mRNA expression in HGF (Montrer HGF Anticorps) 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 (Montrer TICAM1 Anticorps) TIR dimer.

9. induction of both IL-6 (Montrer IL6 Anticorps) and IL-8 (Montrer IL8 Anticorps) is associated with elevated TIRAP (Montrer TIRAP Anticorps) and reduced TRAM (Montrer TRAM1 Anticorps) 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 (Montrer OVA Anticorps) 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 (Montrer RNF138 Anticorps) as key mediator of this phenomenon.

2. the present study indicated that MyD88 (Montrer MYD88 Anticorps) and TRIF (Montrer RNF138 Anticorps) 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 (Montrer TLR4 Anticorps)) application induces proliferation of dormant hematopoietic stem cells (HSC (Montrer FUT1 Anticorps)) and impairs HSC (Montrer FUT1 Anticorps) self-renewal via TLR4 (Montrer TLR4 Anticorps)-TRIF (Montrer RNF138 Anticorps)-ROS (Montrer ROS1 Anticorps)-p38 (Montrer CRK Anticorps) signaling.

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

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

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

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

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

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

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