I-TAC/CXCL11 Protein, Human

CXCL11, also known as IFN-inducible T-cell α-chemoattractant (I-TAC), belongs to the ELR-negative CXC chemokine family. CXCL11 is produced by a variety of cells including leukocytes, fibroblasts, and endothelial cells upon stimulation with interferons (IFNs). CXCL11 signals through CXCR3. CXCL11 is associated with pleiotropic functions including chemotactic migration, regulation of cell proliferation and self-renewal, increasing cell adhesion, and modulation of angiostatic effects^[1][2]. I-TAC/CXCL11 Protein, Human consists of 73 amino acids (F22-F94) and is expressed in E. coli.

CXCL11 is mainly expressed in the lung, pancreas, thymus, peripheral blood leukocytes, spleen, and liver and is expressed at lesser levels in the intestine, placenta, and prostate. CXCL11 is located on human chromosome 4 and is mainly secreted by cancer cells, leukocytes, monocytes, dendritic cells, endothelial cells, and fibroblasts. CXCL11 attracts activated lymphocytes and NK cells to inflamed tissue and to tumors and inhibits the generation of novel blood vessels essential for tumor growth and tissue repair^[1][2].
CXCL11 which can bind to two different chemokine receptors, CXCR3 and CXCR7. CXCL11 is characterized by the presence of 1 amino acid in between the 2 NH2-terminal cysteines. CXCL11 is usually expressed at low levels in homeostatic conditions, but is upregulated during cancer or infectious disease processes. CXCL11 is mainly induced by IFN-γ and IFN-β and is weakly induced by IFN-α. CXCL11 has potent chemoattractant activity for IL-2 activated T cells and transfected cell lines expressing CXCR3, but not freshly isolated T cells, neutrophils or monocytes. Simultaneous stimulation of fibroblasts or endothelial cells with IFN-γ and interleukin-1β or the TLR3 ligand double-stranded RNA resulted in a synergistic increase of CXCL11 production. In leukocytes, bacterial LPS and PGN even inhibited interferon-induced CXCL11 production. CXCL11 attracts activated T-helper 1 (Th1) lymphocytes and natural killer (NK) cells. Furthermore, CXCL11 can bind to CXCR7, which is associated with invasiveness and reduces apoptosis of tumor cells^[1][2].
The diverse functions of CXCL11 include inhibiting angiogenesis, affecting the proliferation of different cell types, playing a role in fibroblast directed carcinoma invasion, increasing adhesion properties, suppressing M2 macrophage polarization, and facilitating the migration of certain immune cells^[1][2].

Recombinant human CXCL11 (100 ng/mL) promotes proliferation and migration of IGROV-1 cells via CXCR3. Recombinant human CXCL11 (100 ng/mL; 5-60 min) increases the phosphorylated p44/42 and phosphorylated Akt in ovarian cancer cells^[3].

1. The ED₅₀ is <2.5 μg/mL as measured by CHO cells, corresponding to a specific activity of >400 units/mg.
2. The biological activity determined by a chemotaxis bioassay using activated human T-lymphocytes. The ED₅₀ for this effect is 1.98 ng/mL in the presence of 1 ng/mL human IL-2, corresponding to a specific activity is 5.05×10^5 U/mg.

• 
  The biological activity determined by a chemotaxis bioassay using activated human T-lymphocytes. The ED₅₀ for this effect is 1.98 ng/mL in the presence of 1ng/mL human IL-2, corresponding to a specific activity is 5.05×10⁵ U/mg.

Human

E. coli

Tag Free

O14625 (F22-F94)

6373  [NCBI]

FPMFKRGRCLCIGPGVKAVKVADIEKASIMYPSNNCDKIEVIITLKENKGQRCLNPKSKQARLIIKKVERKNF

Approximately 10.71 kDa

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

Lyophilized powder.

Lyophilized from a 0.2 μm filtered solution of PBS or 20 mM PB, 150 mM NaCl, pH 7.4.

<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]. Proost P, et al. Proteolytic processing of CXCL11 by CD13/aminopeptidase N impairs CXCR3 and CXCR7 binding and signaling and reduces lymphocyte and endothelial cell migration. Blood. 2007 Jul 1;110(1):37-44.  [Content Brief]

  [2]. Proost P, et al. Proteolytic processing of CXCL11 by CD13/aminopeptidase N impairs CXCR3 and CXCR7 binding and signaling and reduces lymphocyte and endothelial cell migration. Blood. 2007 Jul 1;110(1):37-44.  [Content Brief]

  [3]. Qun Gao, et al. CXCL11 Signaling in the Tumor Microenvironment. Adv Exp Med Biol. 2021;1302:41-50.  [Content Brief]

  [4]. Tat-San Lau, et al. Cancer cell-derived lymphotoxin mediates reciprocal tumour-stromal interactions in human ovarian cancer by inducing CXCL11 in fibroblasts. J Pathol. 2014 Jan;232(1):43-56.  [Content Brief]