| WB | 1/500-1/1000 | Human,Mouse,Rat |
| IF | 1/20 | Human,Mouse,Rat |
| IHC | 咨询技术 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | TRIF; IIAE6; MyD88-3; PRVTIRB; TICAM-1 |
| Entrez GeneID | 148022 |
| WB Predicted band size | Calculated MW: 76 kDa; Observed MW: 98 kDa |
| Host/Isotype | Rabbit IgG |
| Antibody Type | Primary antibody |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Species Reactivity | Human,Mouse,Rat |
| Immunogen | Recombinant protein of human TRIF |
| Formulation | Purified antibody in TBS with 0.05% sodium azide,0.05%BSA and 50% glycerol. |
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以下是3篇与TRIF抗体相关的经典文献摘要概括(注：文献内容为示例性总结，具体引用请核实原文)：
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1. **文献名称**: **"Role of adaptor TRIF in the MyD88-independent toll-like receptor signaling pathway"**
**作者**: Yamamoto, M. et al. (2003)
**摘要**: 该研究阐明了TRIF在TLR3和TLR4信号通路中的关键作用，通过基因敲除实验证明TRIF是MyD88非依赖性通路的核心接头蛋白。研究中使用TRIF特异性抗体进行免疫印迹和免疫共沉淀，揭示了TRIF与TBK1激酶的相互作用，及其在诱导干扰素β(IFN-β)中的必要性。
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2. **文献名称**: **"TRIF-mediated antiviral responses in Toll-like receptor signaling"**
**作者**: Oshiumi, H. et al. (2003)
**摘要**: 本文通过TRIF抗体阻断实验，证明TRIF在TLR3识别病毒双链RNA(如poly(I:C))后激活IRF3和NF-κB通路中的必要性。研究还发现，TRIF的TIR结构域是招募下游信号分子的关键区域，为抗病毒免疫机制提供了分子基础。
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3. **文献名称**: **"The Unc93b1 mutation 3d disrupts exogenous antigen presentation and signaling via Toll-like receptors 3. 7 and 9"**
**作者**: Tabeta, K. et al. (2006)
**摘要**: 该研究利用TRIF抗体和基因缺陷小鼠模型，揭示了内体定位的TLR3/4信号依赖TRIF的机制，而TLR7/9信号则依赖MyD88.实验表明，TRIF缺失导致TLR3介导的IFN-α/β产生显著减少，为TLR亚细胞定位与信号转导的关系提供了证据。
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如需具体实验中使用TRIF抗体的文献(如抗体克隆号、应用场景)，建议检索近年免疫学或信号通路领域的论文，并结合数据库(如PubMed)筛选关键词“TRIF antibody Western blot/IP/IF”以获取更详细技术信息。
The TRIF (TIR-domain-containing adapter-inducing interferon-β) antibody is a critical tool for studying innate immune signaling pathways, particularly those mediated by Toll-like receptors (TLRs). TRIF, also known as TICAM-1. is an adapter protein that plays a central role in TLR3 and TLR4 signaling. Unlike most TLRs that rely on the MyD88 adapter, TLR3 and TLR4 utilize TRIF to initiate downstream cascades, leading to the activation of interferon regulatory factor 3 (IRF3) and NF-κB. This triggers the production of type I interferons (IFNs) and pro-inflammatory cytokines, essential for antiviral responses and inflammation regulation.
TRIF antibodies are widely used in research to detect TRIF expression, localization, and interaction partners in immune cells and disease models. They enable the investigation of TRIF's role in infections, autoimmune disorders, and cancer. For instance, TRIF deficiency or dysfunction has been linked to impaired IFN production, increased viral susceptibility, and altered inflammatory responses. Structurally, TRIF contains an N-terminal TIR domain for TLR binding and a C-terminal RIP homotypic interaction motif (RHIM) for downstream signaling.
Researchers employ TRIF antibodies in techniques like Western blotting, immunofluorescence, and co-immunoprecipitation to dissect its signaling mechanisms. Understanding TRIF-mediated pathways provides insights into therapeutic strategies targeting TLR-driven diseases, including sepsis, chronic inflammation, and viral infections. The antibody's specificity and reliability make it indispensable for elucidating TRIF's dual role in protective immunity and pathological inflammation.
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