| WB | 1/1000 | Human,Mouse,Rat |
| IF | 咨询技术 | 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 | Butyrophilin subfamily 3 member A1, CD277, BTN3A1, BTF5 |
| Entrez GeneID | 11119 |
| WB Predicted band size | 57.7kDa |
| 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 |
| Immunogen | This BTN3A1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 345-374 amino acids from the C-terminal region of human BTN3A1. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
+ +
以下是关于 **BTN3A1抗体** 的3-4篇参考文献示例(文献信息为模拟内容，供参考)：
---
1. **文献名称**: *"BTN3A1 mediates γδ T cell activation by phosphoantigens"*
**作者**: Vavassori, S. et al.
**摘要**: 本研究揭示了BTN3A1在γδ T细胞识别磷酸抗原(如HMBPP)中的关键作用，证明其抗体阻断可抑制Vγ9Vδ2 T细胞的活化，提示BTN3A1作为磷酸抗原传感器的功能。
2. **文献名称**: *"Structural basis for BTN3A1 in immune regulation through phosphoantigen recognition"*
**作者**: Harly, C. et al.
**摘要**: 通过晶体结构分析，阐明BTN3A1胞内B30.2结构域与磷酸抗原结合机制，并利用抗体实验验证其与TCR的相互作用，为靶向BTN3A1的免疫疗法提供依据。
3. **文献名称**: *"Antibody blockade of BTN3A1 enhances antitumor immunity by promoting T cell activation"*
**作者**: Sandstrom, A. et al.
**摘要**: 研究显示，抗BTN3A1单克隆抗体可通过解除免疫抑制信号，增强CD8+ T细胞和γδ T细胞的肿瘤杀伤能力，在黑色素瘤模型中显著抑制肿瘤生长。
4. **文献名称**: *"BTN3A1 governs antigen presentation and T cell co-stimulation in dendritic cells"*
**作者**: Rigau, M. et al.
**摘要**: 发现BTN3A1在树突状细胞中调控抗原呈递和共刺激分子表达，其抗体阻断可抑制T细胞增殖，提示其在自身免疫疾病中的潜在治疗价值。
---
(注：以上文献为示例，实际引用需以真实发表文章为准。)
BTN3A1 (Butyrophilin Subfamily 3 Member A1), also known as CD277. is a transmembrane glycoprotein belonging to the butyrophilin family, which plays a role in immune regulation. It is primarily expressed on immune cells, epithelial cells, and certain cancer cells. Structurally, BTN3A1 contains immunoglobulin (Ig)-like domains in its extracellular region and a cytoplasmic B30.2 domain, which is critical for its interaction with intracellular phosphoantigens.
Functionally, BTN3A1 is a key mediator in γδ T cell activation. It binds to phosphoantigens (e.g., microbial or tumor-derived metabolites) via its intracellular domain, triggering conformational changes that enable interaction with the γδ T cell receptor (TCR). This activation pathway is crucial for bridging innate and adaptive immunity, particularly in infection control and tumor surveillance. Dysregulation of BTN3A1 has been implicated in autoimmune diseases and cancer immune evasion.
BTN3A1-targeting antibodies are tools for studying its biological roles or modulating immune responses. Agonistic antibodies can mimic phosphoantigen-induced activation, enhancing γδ T cell-mediated antitumor activity, while blocking antibodies may suppress excessive inflammation. These antibodies are also explored in diagnostics to assess BTN3A1 expression in cancers, where overexpression correlates with disease progression. Current research focuses on optimizing antibody specificity and therapeutic efficacy, though challenges remain in understanding its precise signaling mechanisms and cross-talk with other immune checkpoints like PD-1/PD-L1.
×
