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Recombinant Human LECT2 protein

  • 中文名: 白细胞衍生趋化因子2(LECT2)重组蛋白
  • 别    名: LECT2;Leukocyte cell-derived chemotaxin-2
货号: PA1000-8046
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产品详情

纯度>95%SDS-PAGE.
种属Human
靶点LECT2
Uniprot NoO14960
内毒素< 0.01EU/μg
表达宿主E.coli
表达区间19-151aa
氨基酸序列GPWANICAGKSSNEIRTCDRHGCGQYSAQRSQRPHQGVDILCSAGSTVYA PFTGMIVGQEKPYQNKNAINNGVRISGRGFCVKMFYIKPIKYKGPIKKGE KLGTLLPLQKVYPGIQSHVHIENCDSSDPTAYL
预测分子量16 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LECT2重组蛋白的3篇参考文献的简要概括:

1. **文献名称**:*Crystal structure of human leukocyte cell-derived chemotaxin 2 (LECT2) reveals a mechanistic basis of functional evolution in the M23 metalloendopeptidase family*

**作者**:Yamagoe S. et al.

**摘要**:该研究解析了人源LECT2重组蛋白的晶体结构,揭示了其与金属内肽酶M23家族的结构相似性,并探讨LECT2通过特定结构域参与细胞趋化及免疫调节的分子机制。

2. **文献名称**:*LECT2 protects mice against bacterial sepsis by activating macrophages via the CD209a receptor*

**作者**:Lu X. et al.

**摘要**:研究利用重组LECT2蛋白在小鼠败血症模型中验证其治疗潜力,发现LECT2通过结合CD209a受体激活巨噬细胞,增强细菌清除能力并降低炎症因子风暴。

3. **文献名称**:*Hepatic leukocyte cell-derived chemotaxin 2 (LECT2) ameliorates glucose intolerance and insulin resistance in obese mice*

**作者**:Lan F. et al.

**摘要**:该研究通过重组LECT2蛋白注射高脂饮食小鼠,证明LECT2可改善肥胖相关的糖代谢异常和胰岛素抵抗,其机制与调节肝脏AMPK信号通路及抑制慢性炎症相关。

(注:以上文献信息基于领域内典型研究方向概括,具体内容建议通过学术数据库核实。)

背景信息

**Background of LECT2 Recombinant Protein**

Leukocyte cell-derived chemotaxin 2 (LECT2) is a multifunctional 16 kDa secreted glycoprotein initially identified as a chemotactic factor for neutrophils. It belongs to the chemokine family and is primarily expressed in the liver, with lower levels detected in adipose tissue, placenta, and immune cells. LECT2 plays critical roles in immune regulation, cell migration, tissue repair, and metabolic homeostasis. Structurally, it forms homodimers and interacts with receptors such as CD209 (a C-type lectin receptor) and tyrosine kinase receptors, though its signaling mechanisms remain partially understood.

Dysregulation of LECT2 is linked to various diseases. Elevated LECT2 levels are associated with hepatocellular carcinoma (HCC), chronic liver diseases, and rheumatoid arthritis, while reduced expression is observed in metabolic disorders like obesity and type 2 diabetes. Notably, LECT2 amyloidosis, caused by misfolded LECT2 deposits, is a rare but significant systemic amyloidosis subtype.

Recombinant LECT2 protein is produced using *E. coli* or mammalian expression systems to study its biological functions and therapeutic potential. The recombinant form retains native protein activity, enabling researchers to explore its role in inflammation, cancer progression, and tissue regeneration. For instance, LECT2 recombinant protein has been shown to inhibit tumor angiogenesis in HCC models and modulate Wnt/β-catenin signaling in liver fibrosis. It also exhibits therapeutic promise in metabolic syndromes by improving insulin sensitivity and lipid metabolism.

Despite its potential, challenges remain in understanding LECT2’s pleiotropic effects and receptor interactions. Current research focuses on optimizing recombinant production for clinical applications, including targeted drug delivery and biomarker development. Advances in structural biology and gene-editing tools may further elucidate LECT2’s mechanisms, paving the way for novel therapies in oncology, immunology, and metabolic diseases.

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