Cat. Number |
CXCL9
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Chemical Name |
CXCL9 Protein, Human, Recombinant
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Qty 1 |
20µg
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References |
名称: CXCL9 纯度:> 90 % 宿主:E. coli 种属:Human 生物活性: Testing in progress 蛋白构建: A DNA sequence encoding the human CXCL9 (Q07325) (Thr 23-Thr 125) was expressed and purified. 分子量: The recombinant human CXCL9 comprises 104 amino acids and has a calculated molecular mass of 11.9 kDa. It migrates as an approximately 16 kDa band in SDS-PAGE under reducing conditions. CXCL9/MIG是趋化因子受体CXCR3的三种配体之一,CXCR3是一种主要存在于T细胞上的G蛋白偶联受体。CXCL9/MIG,连同CXCL1和CXCL11,可以通过绑定激活CXCR3。CXCL9是一种细胞因子,影响参与免疫和炎症反应的细胞的生长、运动或活化状态。 上海惠诚生物提供CXCL9 Protein, Human, Recombinant 以及各类细胞因子,同时推出CHO稳定细胞株开发技术服务方案,详情咨询电话17715331663 QQ:2303607288 CXCL9 Background Information: Chemokine (C-X-C motif) ligand 9 (CXCL9), also known as Monokine induced by gamma interferon (MIG), is a small cytokine belonging to the CXC chemokine family. The function of this chemokine has not been specifically defined; however, it is thought to be involved in T cell trafficking. CXCL9/MIG functions as one of the three ligands of chemokine receptor CXCR3 which is a G protein-coupled receptor found predominantly on T cells. CXCL9/MIG, together with CXCL1 and CXCL11, may activate CXCR3 by binding to it. CXCL9 serves as a cytokine that affects the growth, movement, or activation state of cells that participate in immune and inflammatory response. It has been observed that tumour endothelial cells secrete high levels of CXCL9 in all, and CXCL1 in most melanoma metastases. Experiment data represent novel mechanisms by which tumour cells in melanoma metastases might use the chemokine-expressing endothelium to leave the tumour and eventually to form additional metastases at distinct sites. Experiment results also improved that CXCL9/MIG plays an important role in CD4+ T lymphocyte recruitment and development of CAV, MOMA-2+ macrophages are the predominant recipient-derived source of CXCL9/MIG, and recipient CD4 lymphocytes are necessary for sustained CXCL9/MIG production and CAV development in this model. Neutralization of the chemokine CXCL9/MIG may have therapeutic potential for the treatment of chronic rejection after heart transplantation.
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