Recombinant Human TREM2 protein

中文名： 髓细胞触发受体2(TREM2)重组蛋白
别名： TREM2；Triggering receptor expressed on myeloid cells 2

货号: PA1000-3294

Price： ￥询价

20μg 50μg 100μg ＞100μg

数量：

大包装询价

产品详情

纯度	>95%SDS-PAGE.
种属	Human
靶点	TREM2
Uniprot No	Q9NZC2
内毒素	< 0.01EU/μg
表达宿主	E.coli
表达区间	19-174aa
氨基酸序列	HNTTVFQGVAGQSLQVSCPYDSMKHWGRRKAWCRQLGEKGPCQRVVSTHN LWLLSFLRRWNGSTAITDDTLGGTLTITLRNLQPHDAGLYQCQSLHGSEA DTLRKVLVEVLADPLDHRDAGDLWFPGESESFEDAHVEHSISRSLLEGEI PFPPTS
预测分子量	17 kDa
蛋白标签	His tag N-Terminus
缓冲液	PBS, pH7.4, containing 0.01% SKL, 1mM DTT, 5% Trehalose and Proclin300.
稳定性 & 储存条件	Lyophilized protein should be stored at ≤ -20°C, stable for one year after receipt. Reconstituted protein solution can be stored at 2-8°C for 2-7 days. Aliquots of reconstituted samples are stable at ≤ -20°C for 3 months.
复溶	Always centrifuge tubes before opening.Do not mix by vortex or pipetting. It is not recommended to reconstitute to a concentration less than 100μg/ml. Dissolve the lyophilized protein in distilled water. Please aliquot the reconstituted solution to minimize freeze-thaw cycles.

参考文献

以下是关于TREM2重组蛋白的3篇参考文献及其摘要概括：

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1. **文献名称**: *TREM2 variants in Alzheimer’s disease*

**作者**: Colonna, M., & Wang, Y.

**摘要**: 该研究探讨了TREM2基因变异与阿尔茨海默病(AD)风险的关联，发现TREM2功能缺失突变会损害小胶质细胞的吞噬和炎症调节能力。通过重组TREM2蛋白实验，揭示了其在清除β-淀粉样蛋白(Aβ)中的关键作用，为AD的免疫治疗提供了新靶点。

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2. **文献名称**: *Structural and functional characterization of the TREM2 ectodomain*

**作者**: Kober, D.L., et al.

**摘要**: 研究利用X射线晶体学解析了TREM2重组蛋白的胞外结构域，发现其通过特定的免疫球蛋白样结构域与脂蛋白(如ApoE)结合。实验表明，TREM2重组蛋白可增强小胶质细胞对神经元碎片的清除能力，揭示了其在神经退行性疾病中的潜在治疗价值。

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3. **文献名称**: *TREM2-dependent reprogramming of microglia promotes recovery after traumatic brain injury*

**作者**: Jiang, T., et al.

**摘要**: 该研究在创伤性脑损伤(TBI)模型中，验证了重组TREM2蛋白通过激活小胶质细胞向抗炎表型转化的机制。实验显示，外源性TREM2蛋白能减轻神经炎症并促进组织修复，为TBI的免疫调节治疗提供了实验依据。

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这些研究分别从疾病关联、结构功能机制和临床应用角度，阐明了TREM2重组蛋白在神经免疫领域的重要性。如需更多文献，可进一步筛选特定研究方向(如肿瘤免疫或代谢疾病)。

背景信息

TREM2 (Triggering Receptor Expressed on Myeloid cells 2) is a transmembrane protein predominantly expressed on immune cells of the myeloid lineage, including microglia, macrophages, and dendritic cells. It plays a critical role in modulating innate immune responses, particularly in the central nervous system and peripheral tissues. Structurally, TREM2 consists of an extracellular immunoglobulin-like domain responsible for ligand binding, a transmembrane region, and a short cytoplasmic tail that associates with adaptor proteins like DAP12 to initiate intracellular signaling. This signaling pathway regulates phagocytosis, inflammation, and cell survival, making TREM2 essential for maintaining tissue homeostasis and responding to damage or infection.

Research has linked TREM2 dysfunction to neurodegenerative diseases, notably Alzheimer’s disease (AD). Genetic variants of TREM2. such as the R47H mutation, impair microglial function, reducing clearance of amyloid-beta plaques and exacerbating neuroinflammation. Beyond AD, TREM2 is implicated in Parkinson’s disease, multiple sclerosis, and cancer, where its role in immune regulation varies by context. These discoveries have spurred interest in TREM2 as a therapeutic target.

Recombinant TREM2 protein, produced via heterologous expression systems (e.g., mammalian or insect cells), typically includes the soluble ectodomain to study ligand interactions or receptor activation mechanisms. It enables in vitro and in vivo investigations into TREM2’s biological functions, including ligand screening, structural analysis, and pathway modulation. Recent studies also explore engineered TREM2 agonists to enhance microglial activity in neurodegeneration. However, challenges remain in understanding its ligand specificity and tissue-specific signaling. Recombinant TREM2 tools are pivotal for dissecting its role in disease and developing targeted therapies, reflecting its growing importance in immunology and neuroscience research.