CCL24/Eotaxin-2 蛋白, Mouse (HEK293, His)

CCL24/Eotaxin-2 Protein, Mouse (HEK293, His) is a CC chemokine that interacts with the chemokine receptor CCR3 to induce eosinophil chemotaxis and mediate atopic diseases, parasitic infections and systemic diseases, as well as promote cellular transport and regulate inflammatory and fibrotic activities. CCL24/Eotaxin-2 Protein, Mouse (HEK293, His) is a recombinant mouse CCL24/Eotaxin-2 (V27-V119) protein expressed by HEK293 with a his tag at the N-terminus^[1].

CCL24，也称为嗜酸性粒细胞趋化蛋白 2 (eotaxin-2) 和骨髓祖细胞抑制因子 2 (MPIF-2)，是 CC 趋化因子家族的一种小细胞因子，位于人类基因组中的第 7 号染色体上。CCL24 对静息 T 淋巴细胞和嗜酸性粒细胞具有高度趋化活性，对中性粒细胞具有较低趋化活性，但对单核细胞和活化淋巴细胞没有趋化活性。通过与其唯一受体CCR3结合，其中CCR3主要存在于嗜酸性粒细胞上，但也存在于嗜碱性粒细胞、单核细胞、Th2淋巴细胞、上皮细胞和气道平滑肌上。CCL24 主要介导特应性疾病、寄生虫感染和全身性疾病，但也促进细胞运输并调节炎症和纤维化活动^[1][2]。

CCL24 deficiency leads to reduced dermal thickness and infiltration of immune cells into the bronchoalveolar lavage (BAL) fluid and significantly reduced α-SMA expression in a mouse model of bleomycin (BLM)-induced skin fibrosis^[3].

Mouse

HEK293

N-His

Q9JKC0 (V27-V119)

56221  [NCBI]

20-30 kDa

Greater than 95% as determined by Tris-Bis PAGE.

溶液.

Supplied as a 0.22 μm filtered solution of 20 mM Tris, 500 mM NaCl, pH 7.5.

<1 EU/μg, determined by LAL method.

N/A.

Stored at -80°C for 1 year. It is stable at -20°C for 3 months after opening. It is recommended to freeze aliquots at -80°C for extended storage. Avoid repeated freeze-thaw cycles.

Shipping with dry ice.

• [1]. Hui Li, et al. Trophoblasts-derived chemokine CCL24 promotes the proliferation, growth and apoptosis of decidual stromal cells in human early pregnancy. Int J Clin Exp Pathol. 2013 May 15;6(6):1028-37.  [Content Brief]

  [2]. Michal Segal-Salto, et al. A blocking monoclonal antibody to CCL24 alleviates liver fibrosis and inflammation in experimental models of liver damage. JHEP Rep. 2020 Jan 2;2(1):100064.  [Content Brief]

  [3]. Adi Mor, et al. Blockade of CCL24 with a monoclonal antibody ameliorates experimental dermal and pulmonary fibrosis. Ann Rheum Dis. 2019 Sep;78(9):1260-1268.  [Content Brief]