Recombinant Human TICAM2
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Product specifications
| Category | Proteins and Peptides |
| Immunogen Target | 1-235 |
| Host | E.Coli |
| Origin | Human |
| Observed MW | 25.7 kDa |
| Expression | Recombinant |
| Purity | Greater than 95% by SDS-PAGE gel analyses |
| Purification | His tag |
| Size 1 | 50μg |
| Size 2 | 200μg |
| Size 3 | 1mg |
| Form | Lyophilized from a 0.2um filtered solution in PBS with 5% trehalose, pH7.4 |
| Tested Applications | Western Blot,ELISA |
| Buffer | Reconstitute with Sterile distilled water |
| Availability | 3-4 weeks |
| Storage | -20°C for 12 months as lyophilized;2-8°C for 1 month under sterile conditions after reconstitution |
| UniProt ID | Q86XR7 |
| Alias | MyD88-4, TICAM-2, TIRAP3, TIRP, TRAM, toll like receptor adaptor molecule 2 |
| Background | Proteins TICAM2 |
| Status | RUO |
| Note | This product is for research use only. |
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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