| ID | Sequence | Length | GC content |
|---|---|---|---|
| AGCGCCCUCAGCGCGCUACGGUCCGCGGGCAACUCCGCAGAAGCCCCAG… | 2541 nt | 0.6297 | |
| AGCGCCCUCAGCGCGCUACGGUCCGCGGGCAACUCCGCAGAAGCCCCAG… | 2499 nt | 0.6311 | |
| AGCGCCCUCAGCGCGCUACGGUCCGCGGGCAACUCCGCAGAAGCCCCAG… | 2107 nt | 0.6251 | |
| AGCGCCCUCAGCGCGCUACGGUCCGCGGGCAACUCCGCAGAAGCCCCAG… | 2684 nt | 0.6300 |
This gene encodes an adaptor protein containing a Toll/interleukin-1 receptor (TIR) homology domain, which is an intracellular signaling domain that mediates protein-protein interactions between the Toll-like receptors (TLRs) and signal-transduction components. This protein is involved in native immunity against invading pathogens. It specifically interacts with toll-like receptor 3, but not with other TLRs, and this association mediates dsRNA induction of interferon-beta through activation of nuclear factor kappa-B, during an antiviral immune response. Mutations in this gene are associated with encephalopathy, acute, infection-induced. [provided by RefSeq, Jul 2020]
A study in humans demonstrated that the TICAM1 was significantly expressed in non-classical monocytes from patients with plaque rupture [Jun Qian et al. DOI:10.3389/fimmu.2022.908815]. In human and mouse models, the TICAM1 was identified as the essential signaling adaptor protein TRIF, which is necessary for the inflammatory cytokine production induced by UVB-damaged self-RNA in keratinocytes and peripheral blood mononuclear cells and for the response to UVB exposure in vivo [Bernard et al. DOI:10.1038/nm.2861]. A study in humans demonstrated that severe trauma induces a unique bone marrow transcriptomic signature characterized by upregulation of genes involved in innate immunity and erythropoiesis inhibition, including components of the TLR4 signaling pathway [Kelly et al. DOI:10.1097/SHK.0000000000001826].