GRO-alpha/CXCL1 Protein, Rat

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, Rat is produced in E. coli, and consists of 72 amino acids (A25-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 rat CXCL1 (1 ng/mL; 24 hours) induces migration of rat granulocytes^[4].

Recombinant rat CXCL1 (1 ng and 10 ng; once) is administered intrathecally into male Wistar rats. The nociceptive threshold is measured after 3, 5, 7, 24 and 48 hours after its administration. CXCL1 induces spinal nociception. CXCL1 would induce mechanical allodynia by activating the spinal microglia and astrocytes^[5].

1. Full biological activity determined by a chemotaxis bioassay using rat neutrophils is in a concentration range of 10-100 ng/mL.
2. Measured in a cell proliferation assay using human umbilical vein endothelial cells. The ED₅₀ this effect is 16.43 ng/mL, corresponding to a specific activity is 6.0864×10⁴ units/mg.

• 
  Measured in a cell proliferation assay using human umbilical vein endothelial cells. The ED₅₀ for this effect is 16.43 ng/mL, corresponding to a specific activity is 6.0864×10⁴ units/mg.

Rat

E. coli

Tag Free

P14095 (A25-K96)

81503  [NCBI]

APVANELRCQCLQTVAGIHFKNIQSLKVMPPGPHCTQTEVIATLKNGREACLDPEAPMVQKIVQKMLKGVPK

7-11 kDa

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

Lyophilized powder.

Lyophilized from a 0.2 μm filtered solution of 20 mM PB, 150 mM NaCl, 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]. 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]. Pascale Ribaux, et al. Induction of CXCL1 by extracellular matrix and autocrine enhancement by interleukin-1 in rat pancreatic beta-cells. Endocrinology. 2007 Nov;148(11):5582-90.  [Content Brief]

  [6]. Thamyris Reis Moraes, et al. Participation of CXCL1 in the glial cells during neuropathic pain. Eur J Pharmacol. 2020 May 15;875:173039.  [Content Brief]