MPIF-1/CCL23 蛋白, Human (P.pastoris, His)

MPIF-1/CCL23 protein, Human (P.pastoris, His), 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 (P.pastoris, His) is a recombinant human MPIF-1/CCL23 (R46-N120) protein expressed by P. pastoris  with a his tag at the C-terminus^[1].

CCL23，也称为巨噬细胞炎症蛋白 3 (MIP-3) 和骨髓祖细胞抑制因子 1 (MPIF-1)，是 CC 趋化因子家族的一种小细胞因子，于 1997 年在源自人主动脉内皮细胞的 cDNA 文库中被鉴定出。位于人类 17 号染色体上。ccl23 与 ccl15 具有一定的氨基酸相似性，并且是唯一具有氨基末端氨基酸被删除的替代剪接变体的趋化因子。由于选择性剪接，CCL23以两种形式出现，较短的CCL23α/CKβ8和较长的CCL23β/CKβ8-1。CCL23在肝、肺、胰腺和骨髓组织中表达，并由单核细胞来源的树突状细胞的组成型释放。ccl23 充当趋化因子，对静息 T 细胞和单核细胞具有高度趋化性，对中性粒细胞具有轻微趋化性。ccl23 主要与趋化因子受体 CCR1（一种跨膜 G 蛋白偶联受体）结合发挥作用。据报道，在体外小鼠和人骨髓干细胞集落形成测定中，CCL23 对粒细胞和单核细胞产生谱系的祖细胞具有剂量依赖性抑制活性。此外，CCL23 在骨形成中发挥作用，是成骨细胞前体的有效化学引诱剂，但对完全分化的成骨细胞或破骨细胞没有影响。ccl23 具有一定的促癌作用，可通过激活血管内皮细胞上的 CCR1 诱导血管生成^[1][4]。

CCL23 (-5 ng/mL, 12 h) up-regulates KDR/Flk-1 mRNA and protein levels in human vascular endothelial cells (HUVECs) at 1 ng/mL by stimulating phosphorylation of SAPK/JNK and ERK. Meanwhile, CCL23 promotes VEGF-induced endothelial proliferation and migration^[2].
CCL23 (-1 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, 1 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 1.% ± 1.1% to 5.8% ± 1.2% and 7.6% ± 1.6% to 2.2% ± .2%, respectively, after 24 hours in NZW rabbit ^[4].

Human

P. pastoris

C-His

P55773-1 (R46-N120)

6368  [NCBI]

Approximately 9.9 kDa.

Greater than 90% as determined by reducing SDS-PAGE

<1 EU/μg, determined by LAL method.

• [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]