Anti-CXCL15 monoclonal antibody (DCABY-4235)


Host Species
Antibody Isotype
Species Reactivity
E. coli-derived recombinant mouse CXCL15/Lungkine. Gln26-Ala167 Accession Number Q9WVL7


Application Notes
Western Blot: 1 μg/mL; ELISA Capture: 2-8 μg/mL; ELISA Detection: 0.1-0.4 μg/mL
We recommend the following for sandwich ELISA (Capture - Detection):
DCABY-4235 - DPABY-533
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.


Alternative Names
CXCL15; chemokine (C-X-C motif) ligand 15; Il8; weche; Scyb15; lungkine
Entrez Gene ID
UniProt ID

Product Background

Chemokine signaling pathway; Cytokine-cytokine receptor interaction;


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Product Name Cat. No. Applications Host Species Datasheet Price Add to Basket


EGCG induces G-CSF expression and neutrophilia in experimental sepsis


Authors: Li, Wei; Wu, Andrew H.; Zhu, Shu; Li, Jianhua; Wu, Rong; D'Angelo, John; Wang, Haichao

A major green tea component, epigallocatechin-3-gallate (EGCG), has been proven protective against lethal sepsis in experimental setting, but its protective mechanisms remain incompletely understood. Here, we provide evidence to support EGCG's capacities in stimulating G-CSF production and neutrophilia in vivo. In an animal model of sepsis, EGCG significantly elevated peritoneal levels of G-CSF and several chemokines (e.g., MCP-1/CCL2 and MIP-1 gamma/CCL9), and consequently increased peritoneal neutrophil numbers (neutrophilia) at a late stage. In vitro, EGCG divergently affected HMGB1-mediated production of several chemokines: reducing CXCL15 and RANTES/CCL5, but elevating G-CSF and MIP-1 alpha/CCL3 production by peritoneal macrophages. Similarly, it significantly induced the expression and secretion of G-CSF and MIP-1 alpha/CCL3 in human peripheral blood mononuclear cells. Based on our preliminary data, it may be important to search for anti-inflammatory and G-CSF-stimulating agents for the clinical management of inflammatory diseases.

TGF beta Signaling in Myeloid Cells Regulates Mammary Carcinoma Cell Invasion through Fibroblast Interactions


Authors: Shaw, Aubie K.; Pickup, Michael W.; Chytil, Anna; Aakre, Mary; Owens, Philip; Moses, Harold L.; Novitskiy, Sergey V.

Metastasis is the most devastating aspect of cancer, however we know very little about the mechanisms of local invasion, the earliest step of metastasis. During tumor growth CD11b(+)Gr1(+) cells, known also as MDSCs, have been shown to promote tumor progression by a wide spectrum of effects that suppress the anti-tumor immune response. In addition to immunosuppression, CD11b(+)Gr1(+) cells promote metastasis by mechanisms that are currently unknown. CD11b(+)Gr1(+) cells localize near fibroblasts, which remodel the ECM and leave tracks for collective cell migration of carcinoma cells. In this study we discovered that CD11b(+)Gr1(+) cells promote invasion of mammary carcinoma cells by increasing fibroblast migration. This effect was directed by secreted factors derived from CD11b(+)Gr1(+) cells. We have identified several CD11b(+)Gr1(+) cell secreted proteins that activate fibroblast migration, including CXCL11, CXCL15, FGF2, IGF-I, IL1Ra, Resistin, and Shh. The combination of CXCL11 and FGF2 had the strongest effect on fibroblast migration that is associated with Akt1 and ERK1/2 phosphorylation. Analysis of subsets of CD11b(+)Gr1(+) cells identified that CD11b(+)Ly6C(high)Ly6G(low) cells increase fibroblast migration more than other myeloid cell populations. Additionally, tumor-derived CD11b(+)Gr1(+) cells promote fibroblast migration more than splenic CD11b(+)Gr1(+) cells of tumor-bearing mice. While TGF beta signaling in fibroblasts does not regulate their migration toward CD11b(+)Gr1(+) cells, however deletion of TGF beta receptor II on CD11b(+)Gr1(+) cells downregulates CXCL11, Shh, IGF1 and FGF2 resulting in reduced fibroblast migration. These studies show that TGF beta signaling in CD11b(+)Gr1(+) cells promotes fibroblast directed carcinoma invasion and suggests that perivascular CD11b(+)Ly6C(high)Ly6G(low) cells may be the stimulus for localized invasion leading to metastasis.

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