MIG/CXCL9 蛋白, Mouse (HEK293, His)

CXCL9, also known as MIG, is one member of the ELR-negative CXC chemokine subfamily, and can be induced by IFN-γ. CXCL9 binds to its receptor CXCR3 and can recruit CXCR3+ cells, such as effector T cells, regulatory T cells (Tregs) and CD8+ cytotoxic T cells. CXCL9 is involved in immunoregulatory and inflammatory processes, but it also play a key role in tumor growth, angiogenesis, and metastasis^[1][2]. MIG/CXCL9 Protein, Mouse (HEK293, His) is produced in HEK293 cells with six C-Terminal His-tags. It consists of 105amino acids (T22-T126).

CXCL9是CXC家族的成员，在免疫细胞的趋化性中具有重要作用。它由多种细胞类型分泌，包括免疫细胞（T淋巴细胞、NK细胞、树突状细胞、巨噬细胞、嗜酸性粒细胞等）和非免疫细胞（肝星状细胞、前脂肪细胞、甲状腺细胞、内皮细胞、肿瘤细胞和成纤维细胞）等)^[1]。
人CXCL9蛋白的氨基酸序列与小鼠和大鼠CXCL9蛋白的同源性较低。
CXCL9是趋化因子受体CXCR3的配体之一介导淋巴细胞浸润至病灶并抑制肿瘤生长。CXCL9吸引CXCR3-（CXCR3-A和CXCR3-B）T淋巴细胞，参与多种生理疾病的发生和维持的发病机制。CXCL9的转录调控是一个涉及许多转录因子的多步骤过程，其中STAT1和NF-κB是两个最有特征的成员。STAT1基因突变和JA/STAT1通路阻断均可降低IFN-γ诱导的CXCL9表达。此外，牙龈卟啉单胞菌可通过降低STAT1-IRF-1转录激活途径成分的水平来抑制CXCL9的表达，从而导致免疫功能下降。脂多糖（LPS）和D-半乳糖胺可诱导STAT1磷酸化并增强CXCL9转录，导致肝脏炎症加剧，甚至导致肝脏凋亡和损伤^[1][2] [3]。
CXCL9可以通过增强肿瘤细胞的迁移和侵袭以及破坏内皮细胞单层来促进癌症转移。然而，作为肿瘤抑制因子，它主要招募肿瘤浸润的CD8+ T细胞和NK细胞，并抑制肿瘤血管生成。此外，IL-12和Th1衍生的IFN-γ通过内源性CXCL9对人伯基特淋巴瘤中肿瘤血管系统的抑制作用发挥抗肿瘤作用。在皮肤T细胞淋巴瘤中，CXCL9在早期表达，但在晚期表达较低。CXCL9 还与人类肝纤维化和小鼠的抗纤维化相关。此外，CXCL9 在冠状动脉粥样硬化斑块中高表达，并特异性招募携带 CXCR3 的 Th1 细胞，从而增加斑块进展和心肌梗死发生的风险^{[1][2]< /sup>[3][4]}。

Recombinant mouse CXCL9 (10 mg/kg; for 4 weeks) is intraperitoneally injected three times a week in the orthotopic murine pancreatic adenocarcinoma (PAAD) model. CXCL9 could significant accelerate the growth of PAAD tumour. CXCL9 promotes PAAD progression and suppresses CD8+ cytotoxic T cells in tumour tissues^[4].

Recombinant mouse CXCL9 (100 ng/mL) displays strong antiproliferative and antimigratory effects on VEGF-stimulated endothelial cells and stellate cells by way of reduced VEGFR2 (KDR), phospholipase Cγ (PLCγ), and extracellular signal-regulated kinase (ERK) phosphorylation^[5].

Mouse

HEK293

C-6*His

P18340 (T22-T126)

17329  [NCBI]

TLVIRNARCSCISTSRGTIHYKSLKDLKQFAPSPNCNKTEIIATLKNGDQTCLDPDSANVKKLMKEWEKKISQKKKQKRGKKHQKNMKNRKPKTPQSRRRSRKTT

18-25 kDa

Greater than 95% as determined by reducing SDS-PAGE

无菌粉末.

Lyophilized from a 0.2 μm filtered solution of PBS, pH 7.4.

<1 EU/μg, determined by LAL method.

It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH₂O. For long term storage it is recommended to add a carrier protein (0.1% BSA, 5% HSA, 10% FBS or 5% Trehalose).

Stored at -20°C for 2 years. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.

Room temperature in continental US; may vary elsewhere.

• [1]. Qiang Ding, et al. CXCL9: evidence and contradictions for its role in tumor progression. Cancer Med. 2016 Nov;5(11):3246-3259.  [Content Brief]

  [2]. Weigang Xiu, et al. CXCL9 secreted by tumor-associated dendritic cells up-regulates PD-L1 expression in bladder cancer cells by activating the CXCR3 signaling. BMC Immunol. 2021 Jan 6;22(1):3.  [Content Brief]

  [3]. Chao-Feng Lin, et al. Potential Effects of CXCL9 and CCL20 on Cardiac Fibrosis in Patients with Myocardial Infarction and Isoproterenol-Treated Rats. J Clin Med. 2019 May 11;8(5):659.  [Content Brief]

  [4]. Hui-Feng Gao, et al. CXCL9 chemokine promotes the progression of human pancreatic adenocarcinoma through STAT3-dependent cytotoxic T lymphocyte suppression. Aging (Albany NY). 2020 Jan 8;12(1):502-517.  [Content Brief]

  [5]. Hacer Sahin, et al. Chemokine Cxcl9 attenuates liver fibrosis-associated angiogenesis in mice. Hepatology. 2012 May;55(5):1610-9.  [Content Brief]