Mouse Toll Like Receptor Adaptor Molecule 1 (TICAM1) Protein

Product specifications

Proteins and Peptides

Toll Like Receptor Adaptor Molecule 1 (TICAM1)

E. coli

Activity: Not tested
Sequence Fragment: Ser263-Val526
Tag: N-terminal His tag

Mouse

Unconjugated

Calculated MW: 32.1 kDa  Observed MW (SDS-PAGE): 39 kDa

Recombinant

> 97%

10 µg

50 µg

100 µg

200 µg

500 µg

Lyophilized

WB, SDS-PAGE

Prior to lyophilization: 100 mM NaHCO<sub>3</sub>, 500 mM NaCl, pH 8.3, containing 1 mM EDTA, 1 mM DTT, 0.01% Sarcosyl, 5% Trehalose and Proclin-300.

Shipped within 5-7 working days.

Store lyophilized form at 2-8°C for up to 1 month. For longer periods, store lyophilized or liquid at -80°C. Avoid repeated freeze–thaw cycles.

No

TICAM1, IIAE6, MyD88-3, PRVTIRB, TICAM-1, TRIF, toll like receptor adaptor molecule 1, TIR domain containing adaptor molecule 1

Protein TICAM1

RUO

THIS PRODUCT IS FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC, THERAPEUTIC OR COSMETIC PROCEDURES. NOT FOR HUMAN OR ANIMAL CONSUMPTION.
Reconstitute in ddH2O to a concentration between 0.1-1.0 mg/ml. Do not vortex.
Concentration: Prior to lyophilization: 200 µg/ml

Descripción

TICAM1, also known as TRIF (TIR-domain-containing adapter-inducing interferon-β), is a key adaptor protein in Toll-like receptor (TLR) signaling, specifically downstream of TLR3 and TLR4. It mediates activation of type I interferon (IFN) responses and pro-inflammatory cytokine production through pathways like IRF3/7 and NF-κB. TICAM1 functions by recruiting downstream signaling molecules, including TBK1, TRAF6, and RIP1, to activate antiviral responses and innate immunity. It is essential for host defense against viral infections, where its activation triggers IFN-β production and inflammatory responses to double-stranded RNA and bacterial components. TICAM1 is widely expressed in immune cells and epithelial tissues, ensuring effective pathogen recognition and elimination. Dysregulation of TICAM1 is associated with immune deficiencies, chronic inflammation, and autoimmune diseases due to impaired or excessive IFN signaling. Knockout studies demonstrate increased susceptibility to viral infections, reduced IFN production, and impaired TLR3/TLR4-mediated immune responses, highlighting its role in antiviral defense and innate immunity.

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