Basic Information

Symbol
TICAM1
RNA class
mRNA
Alias
TIR Domain Containing Adaptor Molecule 1 TICAM-1 PRVTIRB TRIF Proline-Rich, Vinculin And TIR Domain-Containing Protein B Toll-Interleukin-1 Receptor Domain-Containing Adapter Protein Inducing Interferon Beta TIR Domain-Containing Adapter Protein Inducing IFN-Beta Putative NF-Kappa-B-Activating Protein 502H TIR Domain-Containing Adapter Molecule 1 Toll Like Receptor Adaptor Molecule 1 MGC35334 MyD88-3 TIR Domain-Containing Adaptor-Inducing Interferon-Beta TIR Domain Containing Adaptor Inducing Interferon-Beta Toll-Like Receptor Adaptor Molecule 1 IIAE6
Location (GRCh38)
Forensic tag(s)
Other applications

MANE select

Transcript ID
NM_182919.4
Sequence length
2684.0 nt
GC content
0.6300

Transcripts

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
Summary

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]

Forensic Context

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].