Mouse Toll Like Receptor Adaptor Molecule 2 (TICAM2) Protein

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Description
Toll Like Receptor Adaptor Molecule 2 Protein is a recombinant Mouse protein expressed in E. coli.
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Product specifications
Category | Proteins and Peptides |
Immunogen Target | Toll Like Receptor Adaptor Molecule 2 (TICAM2) |
Host | E. coli |
Origin | Mouse |
Conjugation | Unconjugated |
Observed MW | Molecular Weight: Calculated MW: 49.9 kDa Concentration: Prior to lyophilization: 200 µg/ml Sequence Fragment: Ser20-Ser196 Tag: N-terminal His tag and GST tag |
Expression | Recombinant |
Purity | > 95% |
Size 1 | 10 µg |
Size 2 | 50 µg |
Size 3 | 100 µg |
Size 4 | 200 µg |
Size 5 | 500 µg |
Form | Lyophilized To keep the original salt concentration, we recommend reconstituting to the original concentration prior to lyophilization (see Concentration) in ddH2O. If a lower concentration is required, dilute in PBS, pH 7.4. If a higher concentration is required, the product can be reconstituted directly in PBS, pH 7.4, though please note that this will change the overall salt concentration. The stock concentration should be between 0.1-1.0 mg/ml. Do not vortex. |
Tested Applications | WB, SDS-PAGE |
Buffer | Prior to lyophilization: PBS, pH 7.4, containing 0.01% Sarcosyl, 1 mM DTT, 5% Trehalose and Proclin-300. |
Availability | Shipped within 5-7 working days. |
Storage | Store at 2-8 °C for up to one month. Store at -80 °C for up to one year. Avoid repeated freeze/thaw cycles. |
Dry Ice | No |
Alias | MyD88-4, TICAM-2, TIRAP3, TIRP, TRAM, toll like receptor adaptor molecule 2 |
Background | Protein TICAM2 |
Status | RUO |
Note | This product is for research use only. Not for human consumption, cosmetic, therapeutic or diagnostic use. |
Descripción
TICAM2, also known as TRAM (TRIF-related adaptor molecule), is an adaptor protein that functions specifically in Toll-like receptor 4 (TLR4) signaling. It facilitates MyD88-independent pathways, mediating the activation of IRF3 and NF-κB to induce type I interferon and pro-inflammatory cytokine production. TICAM2 acts as a bridge between TLR4 and TICAM1, enabling signaling responses to lipopolysaccharides (LPS) and other pathogen-associated molecular patterns (PAMPs) in Gram-negative bacterial infections. TICAM2 is expressed primarily in immune and epithelial cells, where it contributes to early innate immune responses. Dysregulation of TICAM2 impairs TLR4-mediated IFN-β production and inflammatory signaling, leading to defective immune responses to bacterial infections or chronic inflammation in certain conditions. Knockout studies reveal a loss of MyD88-independent signaling, reduced IRF3 activation, and increased susceptibility to bacterial infections, underscoring its specific and essential role in TLR4 signaling pathways.
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