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抗Human TICAM2 抗体:
抗Rat (Rattus) TICAM2 抗体:
抗Mouse (Murine) TICAM2 抗体:
Human Polyclonal TICAM2 Primary Antibody for IHC (fro), WB - ABIN550261
ONeill, Fitzgerald, Bowie: The Toll-IL-1 receptor adaptor family grows to five members. in Trends in immunology 2003
Show all 2 Pubmed References
Human Polyclonal TICAM2 Primary Antibody for WB - ABIN1169199
Aksoy, Albarani, Nguyen, Laes, Ruelle, De Wit, Willems, Goldman, Goriely: Interferon regulatory factor 3-dependent responses to lipopolysaccharide are selectively blunted in cord blood cells. in Blood 2007
Human Polyclonal TICAM2 Primary Antibody for DB, ELISA - ABIN2747722
Keck, Müller, Fejer, Savic, Tchaptchet, Nielsen, Galanos, Huber, Freudenberg: Absence of TRIF signaling in lipopolysaccharide-stimulated murine mast cells. in Journal of immunology (Baltimore, Md. : 1950) 2011
Data suggest that endosomal localization of TICAM2 is essential for TLR4 (显示 TLR4 抗体)-mediated type I interferon-inducing signaling from endosomes; TICAM2 acts as scaffold protein (显示 HOMER1 抗体) and activates TICAM1 (显示 TICAM1 抗体); N-terminal myristoylation allows TICAM2 to anchor to endosomal membrane. (TICAM2 = toll like receptor adaptor molecule-2; TICAM1 (显示 TICAM1 抗体) = toll like receptor adaptor molecule-1 (显示 TICAM1 抗体); TLR4 (显示 TLR4 抗体) = toll-like receptor 4 (显示 TLR4 抗体)) [REVIEW]
Data show that Toll (显示 TLR4 抗体)/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.
Findings were SNPs in TICAM2 (P = 3.6 x 10(-6)) and IL1B (显示 IL1B 抗体) (P = 4.3 x 10(-5)) associated with TB.
TRAM (显示 TRAM1 抗体) plays a role in TLR7 (显示 TLR7 抗体) signaling through a novel signaling axis towards the activation of anti-viral immunity.
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.
A putative TRAF6 (显示 TRAF6 抗体)-binding motif in TRAM (显示 TRAM1 抗体) may mediate a new TRAM (显示 TRAM1 抗体) function in TLR4 (显示 TLR4 抗体) signaling in regulating inflammatory responses, distinct from its bridging TLR4 (显示 TLR4 抗体) and TRIF (显示 TRIM69 抗体). A TRAM (显示 TRAM1 抗体) E183A mutation abolished this.
results suggest TLR adaptor molecules knockdown, such as MyD88 (显示 MYD88 抗体) or TRAM (显示 TRAM1 抗体), can decrease IL-6 (显示 IL6 抗体) and IL-8 (显示 IL8 抗体) mRNA and increase CXCL12 (显示 CXCL12 抗体) mRNA expression in HGF (显示 HGF 抗体) and HPDLF.
The homotypic interaction between TICAM-2 TIR is indispensable to present a scaffold for recruiting the monomeric moiety of the TICAM-1 (显示 TICAM1 抗体) TIR dimer.
induction of both IL-6 (显示 IL6 抗体) and IL-8 (显示 IL8 抗体) is associated with elevated TIRAP (显示 TIRAP 抗体) and reduced TRAM (显示 TRAM1 抗体) mRNA expression
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.
Using ovalbumin (显示 OVA 抗体) 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 (显示 RNF138 抗体) as key mediator of this phenomenon.
the present study indicated that MyD88 (显示 MYD88 抗体) and TRIF (显示 RNF138 抗体) blockades serve notable and equivalent roles in protecting cardiac deterioration from severe sepsis by attenuating cytokine release, reducing neutrophil infiltration and alleviating apoptosis.
lipopolysaccharide (LPS (显示 TLR4 抗体)) application induces proliferation of dormant hematopoietic stem cells (HSC (显示 FUT1 抗体)) and impairs HSC (显示 FUT1 抗体) self-renewal via TLR4 (显示 TLR4 抗体)-TRIF (显示 RNF138 抗体)-ROS (显示 ROS1 抗体)-p38 (显示 CRK 抗体) signaling.
These results indicate a critical role for Ticam2 in SARS (显示 SARS 抗体)-CoV disease, and highlight the importance of host genetic variation in disease responses.
Distinct mechanisms downstream of TLR4 (显示 TLR4 抗体) signaling mediate myelosuppression and hematopoietic stem cell exhaustion during sepsis through unique effects of MyD88 (显示 MYD88 抗体) and TRIF (显示 RNF138 抗体).
these data show that both Myd88 (显示 MYD88 抗体) and TRIF (显示 RNF138 抗体) are necessary for Th17 differentiation in the lungs in response to immunization with lipopolysaccharide
these studies reveal an additional regulatory function of TRIM8 (显示 TRIM8 抗体) in innate immune responses: TRIM8 (显示 TRIM8 抗体) catalyzes polyubiquitination of TRIF (显示 RNF138 抗体), resulting in disruption of TRIF (显示 RNF138 抗体)-TBK1 (显示 TBK1 抗体) interaction
Stimulation of the TLR4 (显示 TLR4 抗体)-TRIF (显示 RNF138 抗体) pathway can protect against the development of allergic airway disease and that a TRIF (显示 RNF138 抗体)-dependent adjuvant effect on CD4 (显示 CD4 抗体)(+) ICOS (显示 ICOS 抗体)(+) T-cell responses may be a contributing mechanism.
Monophosphoryl lipid A stimulation of a TLR4 (显示 TLR4 抗体)-TRIF (显示 RNF138 抗体)-PI3K-Akt (显示 AKT1 抗体) pathway prevents lipopolysaccharide-induced ERK (显示 EPHB2 抗体) activation in the medullar thick ascending limb.
study reporst a key role for TNF (显示 TNF 抗体)/TNFR1 (显示 TNFRSF1A 抗体) in Yersinia-induced cell death of murine macrophages, which occurs despite the blockade of NF-kappaB (显示 NFKB1 抗体) and MAPK (显示 MAPK1 抗体) signaling imposed by Yersinia on infected cells
TIRP is a Toll/interleukin-1 receptor (IL1R\; MIM 147810) (TIR) domain-containing adaptor protein involved in Toll receptor signaling (see TLR4\; MIM 603030).
NF-kappa-B-activating protein 502
, TIR domain-containing adapter molecule 2
, TRIF-related adaptor molecule
, cytoplasmic adaptor
, putative NF-kappa-B-activating protein 502
, toll-like receptor adaptor protein 3
, toll/interleukin-1 receptor (TIR) domain-containing adapter protein
, TRIF-related adapter molecule
, TMED7-TICAM2 readthrough
, TIR domain-containing adapter protein
, TRIF-related adapter molecule TRAM
, Toll-interleukin I receptor domain (TIR)-containing adaptor molecule (TICAM) 2
, toll/interleukin-1 receptor domain-containing protein