Toll Like Receptor Adaptor Molecule 2 (TICAM2) Antibody
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Description
Toll Like Receptor Adaptor Molecule 2 Antibody is a Rabbit Polyclonal against Toll Like Receptor Adaptor Molecule 2.
Documents del producto
Product specifications
| Category | Primary Antibodies |
| Immunogen Target | Toll Like Receptor Adaptor Molecule 2 (TICAM2) |
| Host | Rabbit |
| Reactivity | Mouse |
| Recommended Dilution | WB: 0.01-2 µg/ml, IHC: 5-20 µg/ml, IF/ICC: 5-20 µg/ml. Optimal dilutions/concentrations should be determined by the end user. |
| Clonality | Polyclonal |
| Conjugation | Unconjugated |
| Purification | Purified by antigen-specific affinity chromatography, followed by Protein A affinity chromatography. |
| Size 1 | 100 µl |
| Size 2 | 200 µl |
| Size 3 | 1 ml |
| Form | Liquid |
| Tested Applications | WB, IHC, IF/ICC |
| Buffer | 0.01 M PBS, pH 7.4, containing 0.05% Proclin-300, 50% glycerol. |
| Availability | Shipped within 5-7 working days. |
| Storage | Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles. |
| Dry Ice | No |
| Alias | MyD88-4, TICAM-2, TIRAP3, TIRP, TRAM, toll like receptor adaptor molecule 2 |
| Background | Antibody anti-TICAM2 |
| Status | RUO |
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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