Anti-TRIF / TICAM1

0.5mg/ml if reconstituted with 0.2ml sterile DI water. TICAM1 (TIR domain containing adaptor molecule 1), also known as TRIF, is an adapter in responding to activation of toll-like receptors (TLRs). It mediates the rather delayed cascade of two TLR-associated signaling cascades, where the other one is dependent upon a MyD88 adapter. By genomic sequence analysis, Oshiumi et al. (2003) mapped the TICAM1 gene to chromosome 19p13.3. By coimmunoprecipitation analysis, Oshiumi et al. (2003) showed that TICAM1 interacts specifically with TLR3, but not with other TLRs. Functional analysis showed that the association of TLR3 and TICAM1 mediates dsRNA activation of IFNB, through NFKB, AP1, or IRF3. TICAM1 activation of NFKB was found to occur predominantly through IRAK1 rather than IRAK2. Small interfering (si)RNA blockage of TICAM1, just upstream of the TIR domain, reduced IFNB production in response to dsRNA. Protein function: Involved in innate immunity against invading pathogens. Adapter used by TLR3 and TLR4 (through TICAM2) to mediate NF- kappa-B and interferon-regulatory factor (IRF) activation, and to induce apoptosis. Ligand binding to these receptors results in TRIF recruitment through its TIR domain. Distinct protein- interaction motifs allow recruitment of the effector proteins TBK1, TRAF6 and RIPK1, which in turn, lead to the activation of transcription factors IRF3 and IRF7, NF-kappa-B and FADD respectively. [The UniProt Consortium]