TICAM2 antibody

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Description
Functions as sorting adapter in LPS-TLR4 signaling to regulate the MYD88-independent pathway during the innate immune response to LPS. Physically bridges TLR4 and TICAM1 and functionally transmits LPS-TRL4 signal to TICAM1; signaling is proposed to occur in early endosomes after endocytosis of TLR4. May also be involved in IL1-triggered NF-kappa-B activation, functioning upstream of IRAK1, IRAK2, TRAF6, and IKBKB; however, reports are controversial. Involved in IL-18 signaling and is proposed to function as a sorting adaptor for MYD88 in IL-18 signaling during adaptive immune response. Isoform 2: Proposed to inhibit LPS-TLR4 signaling at the late endosome by interaction with isoform 1 thereby disrupting the association of isoform 1 with TICAM1. May be involved in TLR4 degradation in late endosomes.
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Product specifications
Category | Primary Antibodies |
Immunogen Target | toll-like receptor adaptor molecule 2 (TICAM2) |
Host | Rabbit |
Reactivity | Human |
Recommended Dilution | WB: 1:500-1:2000; IHC: 1:20-1:200 |
Clonality | polyclonal |
Conjugation | Unconjugated |
Isotype | IgG |
Observed MW | 32 kDa |
Purity | ≥95% as determined by SDS-PAGE |
Purification | Immunogen affinity purified |
Size 1 | 100µg |
Form | liquid |
Tested Applications | ELISA, WB, IHC |
Storage | PBS with 0.02% sodium azide and 50% glycerol pH 7.3, -20℃ for 12 months(Avoid repeated freeze / thaw cycles.) |
UniProt ID | Q86XR7 |
Gene ID | 353376 |
Alias | MyD88-4, TICAM-2, TIRAP3, TIRP, TRAM, toll like receptor adaptor molecule 2 |
Background | Antibody anti-TICAM2 |
Status | RUO |
Note | Mol. Weight 32 kDa |
Descripción
TICAM2, also known as TRAM (TRIF-related adaptor molecule), is an adaptor protein that functions specifically in Toll-like receptor 4 (TLR4) signaling. It facilitates MyD88-independent pathways, mediating the activation of IRF3 and NF-κB to induce type I interferon and pro-inflammatory cytokine production. TICAM2 acts as a bridge between TLR4 and TICAM1, enabling signaling responses to lipopolysaccharides (LPS) and other pathogen-associated molecular patterns (PAMPs) in Gram-negative bacterial infections. TICAM2 is expressed primarily in immune and epithelial cells, where it contributes to early innate immune responses. Dysregulation of TICAM2 impairs TLR4-mediated IFN-β production and inflammatory signaling, leading to defective immune responses to bacterial infections or chronic inflammation in certain conditions. Knockout studies reveal a loss of MyD88-independent signaling, reduced IRF3 activation, and increased susceptibility to bacterial infections, underscoring its specific and essential role in TLR4 signaling pathways.
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