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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
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 (显示 TRAM1 抗体) acts as a sorting adaptor not only for TLR4 (显示 TLR4 抗体), but also for TLR2 (显示 TLR2 抗体), to facilitate signaling to IRF7 (显示 IRF7 抗体) at the endosome, which explains how TLR2 (显示 TLR2 抗体) 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.
viral inhibitor peptide of TLR4 (显示 TLR4 抗体) possibly represents a surface domain of A46 that specifically inhibits TLR4 (显示 TLR4 抗体) by masking critical binding sites on MyD88 adaptor (显示 MYD88 抗体)-like and TRIF-related adaptor molecule
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
STING and TRIF (显示 RNF138 抗体) Contribute to Mouse Sepsis, Depending on Severity of the Disease Model
the role of Toll (显示 TLR4 抗体)-like receptor (TLR) 2 (显示 TLR2 抗体), TLR4 (显示 TLR4 抗体), myeloid differentiation response gene 88, and Toll (显示 TLR4 抗体)-IL-1 (显示 IL1A 抗体) receptor domain-containing adaptor-inducing interferon-gamma (显示 IFNG 抗体) (TRIF (显示 RNF138 抗体)), factors critically involved in the TLR signaling pathway, was studied in experimental autoimmune neuritis.
Juniperus rigida Sieb. extract inhibits macrophage inflammatory responses by attenuating TRIF (显示 RNF138 抗体)-dependent signaling and inflammasome activation.
TRIF (显示 RNF138 抗体)-independent pathways can be involved in the downregulation of drug metabolizing enzymes and transporters through TLR4 (显示 TLR4 抗体) and 3. JNK (显示 MAPK8 抗体)-dependent mechanisms likely mediate this downregulation.
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