MPIF-1/CCL23 Protein, Human (99a.a)

MPIF-1/CCL23 protein, Human (99a.a), a CC chemokine, is highly chemotactic for resting T cells and monocytes, mediates inflammatory and immune responses by binding to the chemokine receptor CCR1, inhibits myeloid progenitor cell formation, and has some pro-cancer effects. MPIF-1/CCL23 Protein, Human (99a.a) is a recombinant human MPIF-1/CCL23 (R22-N120) protein expressed by E. coli^[1].

CCL23, also known as macrophage inflammatory protein 3 (MIP-3) and myeloid progenitor inhibitory factor 1 (MPIF-1), is a small cytokine of the CC chemokine family, identified in 1997 in a cDNA library derived from human aortic endothelial cells and located on human chromosome 17. ccl23 has some amino acid similarity to ccl15 and is the only chemokine with an alternative splice variant in which the amino-terminal amino acid is deleted. Due to selective splicing, CCL23 occurs in two forms, the shorter CCL23α/CKβ8 and the longer CCL23β/CKβ8-1. CCL23 is expressed in liver, lung, pancreas and bone marrow tissues and is released by the constitutive type of monocyte-derived dendritic cells. ccl23 acts as a chemokine and is highly chemotactic for resting T cells and monocytes and slightly chemotactic for neutrophils. ccl23 functions primarily in combination with the chemokine receptor CCR1, a transmembrane G protein-coupled receptor. CCL23 has been reported to have dose-dependent inhibitory activity against progenitors of the granulocyte and monocyte producing lineages in mouse and human bone marrow stem cell colony formation assays in vitro. In addition, CCL23 plays a role in bone formation and is a potent chemoattractant for osteoblast precursors but has no effect on fully differentiated osteoblasts or osteoclasts. ccl23 has some pro-oncogenic effects and induces angiogenesis by activating CCR1 on vascular endothelial cells^[1][4].

CCL23 (0-50 ng/mL, 12 h) up-regulates KDR/Flk-1 mRNA and protein levels in human vascular endothelial cells (HUVECs) at 10 ng/mL by stimulating phosphorylation of SAPK/JNK and ERK. Meanwhile, CCL23 promotes VEGF-induced endothelial proliferation and migration^[2].
CCL23 (0-1000 ng/mL, 12 h) enhances expression of matrix metalloproteinases 2 (MMP-2) mRNA and protein levels in endothelial cells in a dose-dependent manner, but no effect on the expression levels of MMP-9, TIMP-1, TIMP-2 and MT1-MMP in HUVECs^[3].

CCL23 (human, 100 μg/kg, intravenously through the marginal ear vein, daily, 3 days) does not affect total circulating leukocyte, polymorphonuclear leukocyte (PMN) and monocyte counts, slows the release of G1 and G2 cells from the bone marrow into the circulation, prolongs the transit time of G1 and G2 cells and reduces the cumulative number of G1 cells in the circulation. In addition, the percentage of banded and segmented PMN in the bone marrow decreases from 10.0% ± 1.1% to 5.8% ± 1.2% and 7.6% ± 1.6% to 2.2% ± 0.2%, respectively, after 240 hours in NZW rabbit ^[4].

The biological activity determined by a chemotaxis bioassay using human T-lymphocytes is in a concentration of 10-50 ng/ml.

Human

E. coli

Tag Free

P55773-1 (R22-N120)

6368  [NCBI]

RVTKDAETEFMMSKLPLENPVLLDRFHATSADCCISYTPRSIPCSLLESYFETNSECSKPGVIFLTKKGRRFCANPSDKQVQVCMRMLKLDTRIKTRKN

Approximately 11.4 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. CC Chemokines in a Tumor: A Review of Pro-Cancer and Anti-Cancer Properties of the Ligands of Receptors CCR1, CCR2, CCR3, and CCR4. Int J Mol Sci. 2020 Nov 9;21(21):8412.  [Content Brief]

  [2]. Kyu Yeon Han, et al. CCL23 up-regulates expression of KDR/Flk-1 and potentiates VEGF-induced proliferation and migration of human endothelial cells. Biochem Biophys Res Commun. 2009 Apr 24;382(1):124-8.  [Content Brief]

  [3]. Son KN, et al. Human CC chemokine CCL23 enhances expression of matrix metalloproteinase-2 and invasion of vascular endothelial cells. Biochem Biophys Res Commun. 2006 Feb 10;340(2):498-504.  [Content Brief]

  [4]. Chih-Horng Shih, et al. CCL23/myeloid progenitor inhibitory factor-1 inhibits production and release of polymorphonuclear leukocytes and monocytes from the bone marrow. Exp Hematol. 2005 Oct;33(10):1101-8.  [Content Brief]