Tir Domain-Containing Adapter Molecule 1 (TICAM1) Reagents

TIR domain-containing adapter molecule 1

Involved in innate immunity against invading pathogens. Adapter used by TLR3, TLR4 (through TICAM2) and TLR5 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. Phosphorylation by TBK1 on the pLxIS motif leads to recruitment and subsequent activation of the transcription factor IRF3 to induce expression of type I interferon and exert a potent immunity against invading pathogens. Component of a multi-helicase-TICAM1 complex that acts as a cytoplasmic sensor of viral double-stranded RNA (dsRNA) and plays a role in the activation of a cascade of antiviral responses including the induction of proinflammatory cytokines.

Herpes simplex encephalitis 4 (HSE4)

Cytoplasmic vesicle, autophagosome. Cytoplasm, cytosol. Mitochondrion.

Ubiquitously expressed but with higher levels in liver.

TICAM1; PRVTIRB; TRIF; TIR domain-containing adapter molecule 1; TICAM-1; Proline-rich, vinculin and TIR domain-containing protein B; Putative NF-kappa-B-activating protein 502H; Toll-interleukin-1 receptor domain-containing adapter protein inducing interferon beta; MyD88-3; TIR domain-containing adapter protein inducing IFN-beta

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.