I-309/CCL1 Protein, Human (CHO)

I-309/CCL1 Protein, Human (CHO) is a cytokine that mediates inflammatory immune responses, viral infections, and tumorigenesis by interacting with the CCR8 chemokine receptor on the cell surface and attracting monocytes, natural killer cells, and immature B-cell nuclear dendritic cells. I-309/CCL1 Protein, Human (CHO) is a recombinant human CCL1 (K24-K96) expressed by CHO^[1].

CCL1 is a small glycoprotein belonging to the CC chemokine family with a molecular weight of approximately 15-16 kDa, known as small inducible cytokine I-309 in humans and TCA-3 in mice. CCL1 is secreted by activated monocytes, macrophages, T lymphocytes and endothelial cells and is chemotactic for monocytes but not for neutrophils^[1].    CCL1 can be activated by interaction with the cell surface chemokine receptor CCR8, which induces Ca²⁺ influx, stimulates transient increases in cytoplasmic free calcium concentration in monocytes, and inhibits apoptosis in thymocyte lines via the RAS/MAPK pathway. Among others, CCR8 is constitutively expressed in monocytes, macrophages, Th2 and regulatory T lymphocytes and is the sole receptor for the human CCL1 and for the viral chemokine, vCCL1 (viral macrophage inflammatory protein 1). CCR8 has been shown to be associated with phagocytic macrophages and activated microglia in MS lesions and is directly related to demyelinating activity^[2].     CCL1 is involved in inflammatory processes through leukocyte recruitment and can play a key role in angiogenesis and other viral and neoplastic processes. A number of single nucleotide polymorphisms (SNPs) in the CCL1 gene have been associated with the progression of chronic obstructive pulmonary disease (COPD). In parallel, CCL1 plays a role in various CNS functions and diseases and may be associated with neuroinflammatory disorders^[3].

CCL1 (100 ng/mL, 3h) stimulates a 14-fold increase in human aortic smooth muscle cells (VSMCs) migration and induces VSMC chemotaxis. Also, it stimulates VSMC secretion of pro - MMP2 and induces MMP-2 mRNA^[4].

1.The ED₅₀ is <1 μg/mL as measured by CHO-K1/Gα15/hCCR8 cells (human Gα15 and human CCR8 stably expressed in CHO-K1 cells).
2.Determined by its ability to chemoattract THP-1 cells. The ED₅₀ for this effect is 22 ng/mL.

Human

CHO

Tag Free

P22362 (K24-K96)

6346  [NCBI]

KSMQVPFSRCCFSFAEQEIPLRAILCYRNTSSICSNEGLIFKLKRGKEACALDTVGWVQRHRKMLRHCPSKRK

Approximately 15 kDa due to the glycosylation.

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

Lyophilized powder

Lyophilized from a 0.22 μm filtered solution of PBS or PBS, pH 7.4, 8% trehalose.

<0.2 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]. M D Miller, et al. The human cytokine I-309 is a monocyte chemoattractant. Proc Natl Acad Sci U S A. 1992 Apr 1;89(7):2950-4.  [Content Brief]

  [2]. Miller MD, et al. The human cytokine I-309 is a monocyte chemoattractant. Proc Natl Acad Sci U S A. 1992 Apr 1;89(7):2950-4.  [Content Brief]

  [3]. A Zingoni, et al. The chemokine receptor CCR8 is preferentially expressed in Th2 but not Th1 cells. J Immunol. 1998 Jul 15;161(2):547-51.  [Content Brief]

  [4]. Roos RS, et al. Identification of CCR8, the receptor for the human CC chemokine I-309. J Biol Chem. 1997 Jul 11;272(28):17251-4.  [Content Brief]

  [5]. Gültekin Tamgüney, et al. Autocrine stimulation of rhadinovirus-transformed T cells by the chemokine CCL1/I-309. Oncogene. 2004 Nov 4;23(52):8475-85.  [Content Brief]

  [6]. Nasreen S Haque, et al. Chemokine receptor-8 (CCR8) mediates human vascular smooth muscle cell chemotaxis and metalloproteinase-2 secretion. Blood. 2004 Feb 15;103(4):1296-304.  [Content Brief]