GRO-alpha/CXCL1 蛋白, Mouse

CXCL1 (Chemokine (C-X-C motif) ligand 1), also known as GRO alpha, NAP-3 or MGSA, belongs to the sub-family of CXC chemokine. CXCL1 is involved in the development of many inflammatory diseases, including the induction of angiogenesis and recruitment of neutrophils. CXCL1 is produced by many cell types, and activates CXCR2 and, at high levels, CXCR1^[1]. GRO-alpha/CXCL1 Protein, Mouse is produced in E. coli, and consists of 72 amino acids (A25-N96).

CXCL1，也称为 GRO-α，是一种最初从人类黑色素瘤细胞中分离出来的多肽。CXCL1 通过与其相应的 G 蛋白偶联受体 CXCR2 特异性结合，充当中性粒细胞的关键化学引诱剂。CXCL1 调节血管生成、肿瘤发生和伤口愈合。一般来说，CXCL1 水平在正常生理条件下极低，而在炎症条件下则大幅升高^[2][3]。
人类 CXCL1 的氨基酸序列小鼠和大鼠CXCL1蛋白同源性较低。
翻译后，合成的CXCL1前体长度为107个氨基酸。信号肽从其 N 末端被去除，从而将前体缩短为 73 个氨基酸。还可以从 C 末端去除另外两个氨基酸。此外，CXCL1 中的所有四个半胱氨酸残基形成两个二硫桥。二硫桥为 CXCL1 提供了适当的结构，这决定了该趋化因子的特性。分泌后，CXCL1 进行进一步的蛋白水解加工，从而调节该趋化因子的活性。从 N 末端去除 3 个、4 个或 5 个氨基酸，分别产生 CXCL1(4-73)、CXCL1(5-73) 和 CXCL1(6-73)。这使 CXCL1 活性增加了 30 倍，这是通过其诱导处理细胞趋化性的能力来衡量的。迄今为止，已经发现了三种CXCL1受体——CXCR1、CXCR2和非典型趋化因子受体1（ACKR1）。通过 NF-κB 激活，IL-1β、TNF-α 和 IL-17 等细胞因子可增加 CXCL1 的表达。CXCL1 可结合成生物活性二聚体，主要通过 CXCR2/IL-8 RB^[1] 发出信号。
CXCL1 表达被致癌物诱导后，通过募集中性粒细胞参与炎症反应。这会导致慢性炎症。除了增加增殖之外，CXCL1 还诱导癌细胞迁移，特别是 EMT。CXCL1由淋巴管内皮细胞（LEC）产生，在淋巴管生成过程中使肿瘤细胞迁移到淋巴管，导致淋巴结转移。CXCL1 是中性粒细胞的趋化因子。此外，它还导致这些细胞从骨髓中动员起来。CXCL1 还可以诱导调节性 T 细胞 (Treg) 和 MSC 招募到肿瘤微环境中。CXCL1 另一个同样重要的特性是其诱导血管生成的能力^[1]。

Recombinant mouse CXCL1 (0.25-250 ng/mL; incubated for 4-6 days) has no effect on CD3 stimulated T cell proliferation^[4].

Recombinant mouse CXCL1 (300 pg; once) is intravenously injected into SCD mice. The results shows that CXCL1 induces acute vaso-occlusive crisis^[5].
Recombinant mouse CXCL1 is injected intra-plantar in the right hindpaws of normal mice 100 ng/15 μL. Intraplantar injection of mouse recombinant CXCL1 induces mechanical allodynia in naive mice, without thermal sensitization^[6].

1.Full biological activity determined by a chemotaxis bioassay using human peripheral blood neutrophils is in a concentration range of 10-100 ng/mL.
2.Measured in a cell proliferation assay using HUVEC. The ED₅₀ for this effect is ≤0.6478 ng/mL, corresponding to a specific activity is ≥1.508×10⁶ units/mg.

• 
  Measured in a cell proliferation assay using HUVEC.The ED₅₀ for this effect is 0.6633ng/mL, corresponding to a specific activity is 1.508×10⁶ units/mg.

Mouse

E. coli

Tag Free

P12850 (A25-K96)

14825  [NCBI]

APIANELRCQCLQTMAGIHLKNIQSLKVLPSGPHCTQTEVIATLKNGREACLDPEAPLVQKIVQKMLKGVPK

Approximately 7.8-9 kDa

• 
  Greater than 95% as determined by reducing SDS-PAGE.

无菌粉末

Lyophilized after extensive dialysis against PBS, pH 7.4 or PBS, pH 7.4, 8% trehalose.

<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]. Jan Korbecki, et al. CXCL1: Gene, Promoter, Regulation of Expression, mRNA Stability, Regulation of Activity in the Intercellular Space. Int J Mol Sci. 2022 Jan 12;23(2):792.  [Content Brief]

  [2]. Dhawan P, et al. Role of CXCL1 in tumorigenesis of melanoma. J Leukoc Biol. 2002 Jul;72(1):9-18.  [Content Brief]

  [3]. Sheng-Mou Hou, et al. CXCL1 contributes to IL-6 expression in osteoarthritis and rheumatoid arthritis synovial fibroblasts by CXCR2, c-Raf, MAPK, and AP-1 pathway. Arthritis Res Ther. 2020 Oct 21;22(1):251.  [Content Brief]

  [4]. Huey-ming Lo, et al. TNF-α induces CXCL1 chemokine expression and release in human vascular endothelial cells in vitro via two distinct signaling pathways. Acta Pharmacol Sin. 2014 Mar;35(3):339-50.  [Content Brief]

  [5]. M Kouwenberg, et al. Reduced CXCL1 production by endogenous IL-37 expressing dendritic cells does not affect T cell activation. PLoS One. 2021 May 24;16(5):e0251809.  [Content Brief]

  [6]. Jung-Eun Jang, et al. CXCL1 and its receptor, CXCR2, mediate murine sickle cell vaso-occlusion during hemolytic transfusion reactions. J Clin Invest. 2011 Apr;121(4):1397-401.  [Content Brief]

  [7]. Yuan Sun, et al. Opioids enhance CXCL1 expression and function after incision in mice. J Pain. 2014 Aug;15(8):856-66.  [Content Brief]