Recombinant Human TICAM2

Background

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.