GRO-alpha/CXCL1 Protein, Mouse (HEK293, His)

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 (HEK293, His) is produced in HEK293 cells with six C-Terminal His-tags. It consists of 77 amino acids (A20-N96).

CXCL1, also known as GRO-α, is a polypeptide that is initially isolated from human melanoma cells. CXCL1 acts as a key chemoattractant for neutrophils by binding specifically to its corresponding G-protein-coupled receptor CXCR2. CXCL1 modulates angiogenesis, tumorigenesis, and wound healing. In general, CXCL1 levels are extremely low under normal physiological conditions and greatly increased during inflammatory conditions^[2][3].
The amino acid sequence of human CXCL1 protein has low homology between mouse and rat CXCL1 protein.
After translation, the synthesized CXCL1 precursor is 107aa long. A signal peptide is removed from its N-terminus, which shortens the precursor to 73aa. Two other amino acids can also be removed from the C-terminus. In addition, two disulfide bridges are formed from all four cysteine residues in CXCL1. The disulfide bridges give the appropriate structure to CXCL1, which determines the properties of this chemokine. After secretion, CXCL1 undergoes further proteolytic processing, which regulates the activity of this chemokine. From the N-terminus, three, four or five amino acids are removed, which produce CXCL1(4-73), CXCL1(5-73), and CXCL1(6-73), respectively. This increases CXCL1 activity 30 times, as measured by its ability to induce the chemotaxis of treated cells. To date, three CXCL1 receptors have been discovered-CXCR1, CXCR2 and atypical chemokine receptor 1 (ACKR1). Through NF-κB activation, CXCL1 expression is increased by cytokines such as IL-1β, TNF-α and IL-17. CXCL1 can associate into bioactive dimers and primarily signals through CXCR2/IL-8 RB^[1].
After CXCL1 expression is induced by carcinogens, it participates in inflammatory responses by recruiting neutrophils. This leads to chronic inflammation. In addition to increasing proliferation, CXCL1 also induces cancer cell migration, particularly EMT. Produced by lymphatic endothelial cells (LECs), CXCL1 enables tumor cell migration into the lymphatic vessels during lymphangiogenesis, leading to lymph node metastasis. CXCL1 is a chemotactic factor for neutrophils. Additionally, it causes the mobilization of these cells from the bone marrow. CXCL1 can also induce recruitment of regulatory T cells (Treg) and MSCs into the tumor niche. Another no-less-important property of CXCL1 is its ability to induce angiogenesis^[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].

Mouse

HEK293

C-6*His

P12850 (R20-K96)

14825  [NCBI]

RLATGAPIANELRCQCLQTMAGIHLKNIQSLKVLPSGPHCTQTEVIATLKNGREACLDPEAPLVQKIVQKMLKGVPK

11-13 kDa

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

Lyophilized powder.

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]. 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]. 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]

  [3]. 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]

  [4]. 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]

  [5]. 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]

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