| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 1/20-1/100 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 1/5000-1/10000 | Human,Mouse,Rat |
| Aliases | IIAE1; UNC93; UNC93B; Unc-93B1 |
| 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 |
| Immunogen | Synthetic peptide of human UNC93B1 |
| Formulation | Purified antibody in PBS with 0.05% sodium azide and 50% glycerol. |
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1. **"UNC93B1 mediates differential trafficking of endosomal TLRs"**
- **作者**: Kim YM, Brinkmann MM, Paquet ME, Ploegh HL
- **摘要**: 研究揭示了UNC93B1在内体TLRs(如TLR3、7、9)选择性转运中的关键作用，通过其磷酸化状态调控TLR信号通路的激活，抗体用于检测UNC93B1与TLR的相互作用及亚细胞定位。
2. **"The Unc93b1 mutation 3d disrupts exogenous antigen presentation and signaling via Toll-like receptors 3. 7 and 9"**
- **作者**: Tabeta K, Hoebe K, Janssen EM et al.
- **摘要**: 发现UNC93B1基因突变(3d)导致TLR3/7/9信号传导缺陷，抗体实验证实其影响抗原呈递细胞对病毒核酸的识别，表明UNC93B1是TLR免疫应答的核心调控分子。
3. **"Structural basis for the interaction between the cytoplasmic domain of UNC93B1 and the TLR3 transmembrane domain"**
- **作者**: Christie DA, Kirchhofer D, Tanji H et al.
- **摘要**: 通过结构生物学手段解析UNC93B1与TLR3跨膜区的结合机制，抗体应用于共免疫沉淀实验，揭示其通过特定结构域介导TLR转运至内体的分子基础。
4. **"UNC93B1 is essential for TLR activation and host defense against bacterial infection"**
- **作者**: Lee BL, Moon JE, Shu JH et al.
- **摘要**: 证实UNC93B1缺失导致TLR(如TLR11/12)信号通路完全阻断，抗体用于体内外功能验证，证明其在抗细菌免疫中的必要性及作为治疗靶点的潜力。
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注：上述文献为概括性示例，实际引用需核对PubMed/Google Scholar等数据库获取准确信息。
UNC93B1 is a transmembrane protein primarily localized in the endoplasmic reticulum and endolysosomal compartments, playing a critical role in regulating the trafficking and activation of endosomal Toll-like receptors (TLRs), particularly TLR3. TLR7. TLR8. and TLR9. These TLRs are essential for detecting microbial nucleic acids and initiating innate immune responses. UNC93B1 binds directly to these TLRs, facilitating their transport from the endoplasmic reticulum to endosomes and ensuring their proper signaling function. Mutations in UNC93B1 have been linked to impaired TLR signaling, increasing susceptibility to viral infections (e.g., herpes simplex encephalitis) and altering autoimmune disease progression.
Antibodies targeting UNC93B1 are vital tools for studying its expression, localization, and interaction with TLRs. They are widely used in techniques like Western blotting, immunoprecipitation, immunofluorescence, and flow cytometry to assess protein levels in immune cells or tissues. Such antibodies help elucidate UNC93B1’s regulatory mechanisms in TLR-mediated immune responses and its role in pathologies, including infections, autoimmune disorders (e.g., systemic lupus erythematosus), and inflammatory diseases. Commercially available UNC93B1 antibodies are often validated in knockout models to ensure specificity. Research using these antibodies has advanced understanding of how UNC93B1 dysfunction contributes to immune dysregulation, offering potential therapeutic targets for modulating excessive TLR signaling.
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