MCP-1/CCL2 蛋白, Mouse (Biotinylated, sf9, His)

MCP-1/CCL2 Protein, Mouse (Biotinylated, sf9, His) is a cytokine belonging to the CC chemokine family that interacts with the CCR2 chemokine receptor on the cell surface to mediate inflammatory immune responses, viral infections, and tumorigenesis. MCP-1/CCL2 Protein, Mouse (Biotinylated, sf9, His) is a biotinylated mouse MCP-1/CCL2 (M1-N148) expressed by  Spodoptera frugiferda(Sf9) with a His tag at the C-terminus^[1].

CCL2，也称为单核细胞趋化蛋白1 (MCP1)，是属于CC趋化因子家族的小细胞因子。CCL2基因位于人类17号染色体的q11.2-q12区域，编码分子量为9-15 kDa的单体多肽，具体取决于糖基化水平。CCL2主要由单核细胞、巨噬细胞和树突状细胞分泌。由单核细胞、巨噬细胞和树突状细胞分泌，血小板源性生长因子是CCL2基因的主要诱导剂。星形胶质细胞和小胶质细胞也被认为是 CCL2^[1] 的来源。CCL2 通过结合和激活 CCR2 发出信号，并诱导强烈的趋化反应和钙离子的细胞内动员。其中，CCL2/CCR2可以通过激活β1整合素和p38-MAPK信号通路来调节巨噬细胞的细胞粘附和趋化性。除了充当化学引诱剂之外，CCL2 还可以通过改变紧密连接 (TJ) 蛋白、调节内皮粘附分子和白细胞整合素的表达以及细胞因子的产生来调节体外脑内皮通透性。此外，CCL2-CCR2 信号传导轴与许多炎症和神经退行性疾病有关，其作用是将炎症细胞招募到 CNS^[2]。CCL2 最初被描述为“肿瘤源性趋化因子”，现已被证明是多种类型免疫细胞的有效趋化因子，也是治疗多种疾病的潜在靶标，例如动脉粥样硬化、多发性硬化症、哮喘、神经性疼痛、糖尿病肾病和癌症^[3]。

MCP-1/CCL2 (1 ng/mL, 24 h) can induce NO production by co-treatment with IFN-γ, increases ERK phosphorylation and increases iNOS expression, suggesting that the mechanism of NO production is related to the ERK1/2 signaling pathway in peritoneal macrophages of mice, thereby increasing bacterial clearance^[3].
CCL2 (.5 ng/μL) promotes α-synuclein secretion and α-synuclein-induced neuronal apoptosis, and induces microglia proliferation and secretion of TNF-α, IL-1β and NO^[4].

MCP-1/CCL2 (intracerebral injection, 5-25 μg, 1 μL/h for 3 days or .5 μL/h for 7 days) induces FITC-albumin leakage at lower concentrations (5-2 μg) but fails or moderately induces leukocyte infiltration. Blood-brain barrier permeability and leukocyte infiltration are significantly increased at 25 μg, and extravasation is significantly enhanced in the treated CD-1 mice compared with the control group 6 h after injection. Prolonged administration for 3 or 7 days results in a significant increase in the percentage of brain water content, and decreases expression of the tight junction proteins occludin, claudin-5, ZO-1 and ZO-2^[2].

Mouse

Sf9 insect cells

C-His

Q5SVU3 (Q24-N148)

20296  [NCBI]

Approximately 27 kDa.

Greater than 95% as determined by reducing SDS-PAGE

<1 EU/μg, determined by LAL method.

• [1]. Qiongyu Hao, et al.  CCL2/CCR2 signaling in cancer pathogenesis. Cell Commun Signal. 2020 May 29;18(1):82.  [Content Brief]

  [2]. Svetlana M Stamatovic, et al. Monocyte chemoattractant protein-1 regulation of blood-brain barrier permeability. J Cereb Blood Flow Metab. 2005 May;25(5):593-606.  [Content Brief]

  [3]. Rachel N Gomes, et al. Bacterial clearance in septic mice is modulated by MCP-1/CCL2 and nitric oxide. Shock. 2013 Jan;39(1):63-9.  [Content Brief]

  [4]. Lijun Zhang, et al. Effect of chemokine CC ligand 2 (CCL2) on α?synuclein?induced microglia proliferation and neuronal apoptosis. Mol Med Rep. 2018 Nov;18(5):4213-4218.  [Content Brief]