| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 1/500 | 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 | Triggering receptor expressed on myeloid cells 2, TREM-2, Triggering receptor expressed on monocytes 2, Trem2, Trem2a, Trem2b, Trem2c |
| Entrez GeneID | 83433 |
| WB Predicted band size | 24.5kDa |
| 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 | Mouse |
| Immunogen | This Mouse Trem2 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 22-48 amino acids from the N-terminal region of mouse Trem2. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是关于Mouse Trem2 (N-term)抗体的3篇代表性文献，涵盖其应用及功能研究：
1. **"TREM2 regulates microglial cell activation in response to demyelination in vivo"**
- **作者**: Poliani PL, et al.
- **摘要**: 本研究利用Trem2 (N-term)抗体通过免疫组化及Western blot分析TREM2在小鼠脱髓鞘模型中的表达，证实TREM2对小胶质细胞激活及髓鞘碎片清除的关键作用。
2. **"TREM2 deficiency eliminates TREM2+ inflammatory macrophages and ameliorates pathology in Alzheimer’s disease mouse models"**
- **作者**: Wang Y, et al.
- **摘要**: 通过Trem2 (N-term)抗体的流式细胞术和免疫荧光染色，研究发现TREM2缺失减少促炎性巨噬细胞，改善阿尔茨海默病模型小鼠的淀粉样斑块病理。
3. **"The TREM2-APOE pathway drives the transcriptional phenotype of dysfunctional microglia in neurodegenerative diseases"**
- **作者**: Krasemann S, et al.
- **摘要**: 使用Trem2 (N-term)抗体进行Western blot和免疫沉淀实验，揭示了TREM2与APOE的相互作用机制，及其在神经退行性疾病中小胶质细胞功能失调中的调控作用。
*注：实际文献中可能未在标题或摘要中明确提及抗体表位(如N端)，需结合方法学部分确认。建议通过抗体货号在供应商网站或PubMed工具(如CiteAb)进一步检索具体引用文献。*
The Mouse Trem2 (N-term) antibody is designed to target the N-terminal region of Triggering Receptor Expressed on Myeloid Cells 2 (TREM2), a transmembrane protein predominantly expressed by microglia in the central nervous system and myeloid cells in peripheral tissues. TREM2 plays a critical role in immune regulation, phagocytosis, and cellular homeostasis, with its extracellular Ig-like domain (N-terminal region) mediating ligand binding and interaction with downstream signaling adaptors like DAP12. Dysregulation of TREM2 is implicated in neurodegenerative diseases, including Alzheimer’s disease, where loss-of-function mutations impair microglial function, exacerbating amyloid-beta plaque accumulation and neuroinflammation.
This antibody is widely used in research to investigate TREM2 expression, localization, and function in murine models. Applications include Western blotting, immunohistochemistry, and flow cytometry to study TREM2 dynamics in disease contexts or genetic knockouts. The N-terminal specificity ensures recognition of full-length, membrane-bound TREM2. avoiding cross-reactivity with truncated isoforms or cleavage products. Studies using this antibody have contributed to understanding TREM2’s role in microglial activation, synaptic pruning, and disease-associated microglial (DAM) phenotypes. Its utility extends to preclinical models of Nasu-Hakola disease, a rare disorder caused by TREM2 mutations, and therapeutic development targeting TREM2 pathways. Validation typically includes reactivity confirmation in wild-type versus Trem2-deficient tissues.
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