recombinant human rh cxcl11  (R&D Systems)

Journal: Molecular Pharmacology

Article Title: Inhibition of constitutive activity of the atypical chemokine receptor 3 by the small-molecule inverse agonist VUF16840

doi: 10.1016/j.molpha.2025.100085

Figure Lengend Snippet: VUF16840 inhibits constitutive as well as agonist induced β -arrestin2 recruitment to ACKR3. (A) Transiently transfected HEK293T cells, expressing hACKR3-SmBiT and β -arrestin2-LgBiT, were stimulated with increasing concentrations CXCL12 or (B) VUF16840. Subsequently, β -arrestin2 recruitment to hACKR3 was detected by NanoBiT complementation. (C) Transfected HEK293T cells were stimulated for 30 minutes with increasing concentrations CXCL12 or VUF16840 and β -arrestin2 recruitment to the hACKR3 was detected by NanoBiT complementation. (D) Transfected HEK293T cells were stimulated with increasing concentrations VUF15485 , VUF16840, CXCL11 or CXCL12, and β -arrestin2 recruitment to hACKR3 was detected by BRET. (E) β -Arrestin2 recruitment to the ACKR3 was measured after stimulation with 100 nM of VUF15485 , CXCL11 or CXCL12 in the presence of increasing concentrations VUF16840. (F) Transfected HEK293T cells were stimulated with increasing concentrations VUF16840 in the presence or absence of 100 nM CXCL12 and β -arrestin2 recruitment to the hCXCR4 was detected by biolumescence resonance energy transfer. Depicted data is normalized as fold-basal and represents the mean ± SD of n experiments with triplicate measurements per experiment. Panel A–C and F depicts the average of 3 experiments; for panel D and E, the number of experiments differed per condition and is summarized in .

Article Snippet: Human recombinant CXCL11 (#CN-13), CXCL12 (#CN-11), and fluorescently labeled CXCL12-A647 (#CAF-11) were purchased from Almac or Protein Foundry.

Techniques: Transfection, Expressing, Förster Resonance Energy Transfer

Journal: Molecular Pharmacology

Article Title: Inhibition of constitutive activity of the atypical chemokine receptor 3 by the small-molecule inverse agonist VUF16840

doi: 10.1016/j.molpha.2025.100085

Figure Lengend Snippet: VUF16840 noncompetitively inhibits agonist-induced β -arrestin2 recruitment to hACKR3. (A) Transiently transfected HEK293T cells, expressing hACKR3-SmBiT and β -arrestin2-LgBiT were stimulated with increasing concentrations of (A) CXCL11 or (B) CXCL12 following a 60 minutes pretreatment with buffer or various concentrations of the inverse agonist VUF16840. Next, the β -arrestin2 recruitment to the hACKR3 was detected by NLuc complementation. Depicted data are the mean ± SD of 3 experiments.

Article Snippet: Human recombinant CXCL11 (#CN-13), CXCL12 (#CN-11), and fluorescently labeled CXCL12-A647 (#CAF-11) were purchased from Almac or Protein Foundry.

Techniques: Transfection, Expressing

Journal: Free radical biology & medicine

Article Title: Oxidative stress-induced decreased expression of FABP5 leads to mitochondrial damage and survival disorder of decidual stromal cells in women with recurrent spontaneous abortion.

doi: 10.1016/j.freeradbiomed.2025.06.003

Figure Lengend Snippet: Fig. 7. FABP5 downregulation in DSCs repressed CXCL11/CXCR3 signaling between DSCs and HTR-8/Svneo cells. (A) KEGG pathway analysis of DEGs identified by RNA-seq in FABP5-knockdown primary DSC. (B) Gene Set Enrichment Analysis (GSEA) of chemokine signaling pathways in FABP5-silenced DSCs. (C) FPKM values of CXCL11 expression in control and FABP5-knockdown groups. (D) RT-qPCR, (E, F) Western blot, and (G) ELISA quantification of CXCL11 expression in DSCs transfected with FABP5-targeting or NC siRNAs. (H) RT-qPCR and (I, J) Western blot analyses of CXCR3 expression in HTR-8/Svneo cells treated with CS from FABP5-deficient or control DSCs. Statistical significance: *P < 0.05, **P < 0.01.

Article Snippet: The concentration of CXCL11 in the CS was measured using a human CXCL11 ELISA kit (Boster, Beijing, China; CAT# EK0737) following the manufacturer’s instructions.

Techniques: RNA Sequencing, Knockdown, Protein-Protein interactions, Expressing, Control, Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay, Transfection

Journal: Cell & bioscience

Article Title: CXCL11 reprograms M2-biased macrophage polarization to alleviate pulmonary fibrosis in mice.

doi: 10.1186/s13578-024-01320-7

Figure Lengend Snippet: Fig. 4 Cytokine analysis of CM from M0, M1, and M2 macrophages. A Comparative analysis of cytokine secretion in CM from naïve and polarized macrophage-CM. Each cytokine was detected in duplicate. Target cytokines are indicated using square frames with numbers. B CXCL9, CXCL11, and PTX3 proteins (indicated by arrows in a panel) were highly detected in M1-CM compared to M0- and M2-CM. C Quantification shows the mean signal intensity

Article Snippet: For recombinant human CXCL11 (R&D SYSTEMS, Minneapolis, Minnesota, USA) treatment, the mice with fibrosis induction received an IV injection of CXCL11 (2 μg/mouse) on days 10, 12, 13, and 15 after BLM administration.

Techniques:

Journal: Cell & bioscience

Article Title: CXCL11 reprograms M2-biased macrophage polarization to alleviate pulmonary fibrosis in mice.

doi: 10.1186/s13578-024-01320-7

Figure Lengend Snippet: Fig. 5 M1 macrophage-derived CXCL11 promotes M2 to M1 phenotype polarization mediated through the p65, ERK1/2, and AKT pathway in vitro. A A schematic diagram illustrating the experimental procedures to examine the effect of CXCL11 on macrophage polarity. B Real-time RT-PCR analyzed the relative mRNA levels of M1 (iNos and Socs3)- and M2 (Arg1 and Mrc1)-related factors. C Western blotting for phosphorylation of p65, ERK1/2, AKT and COX2, iNOS, ARG1, and CD206 protein in BMDM after CXCL11 treatment. α-Tubulin was used as a loading control. D, E The graph shows the relative intensity of phosphorylation of p65, ERK1/2, and AKT (D) and COX2, iNOS, ARG1, and CD206 (E). F A schematic diagram illustrating the experimental procedures to examine the pathway of CXCL11 on macrophage polarity. G Western blotting for phosphorylation of p65, ERK1/2, AKT and COX2, iNOS, ARG1, and CD206 protein in BMDM after CXCL11 treatment with inhibitors. α-Tubulin was used as a loading control. H, I The graph shows the relative intensity of phosphorylation of p65, ERK1/2, and AKT (H) and COX2, iNOS, ARG1, and CD206 (I)

Article Snippet: For recombinant human CXCL11 (R&D SYSTEMS, Minneapolis, Minnesota, USA) treatment, the mice with fibrosis induction received an IV injection of CXCL11 (2 μg/mouse) on days 10, 12, 13, and 15 after BLM administration.

Techniques: Derivative Assay, In Vitro, Quantitative RT-PCR, Western Blot, Phospho-proteomics, Control

Journal: Cell & bioscience

Article Title: CXCL11 reprograms M2-biased macrophage polarization to alleviate pulmonary fibrosis in mice.

doi: 10.1186/s13578-024-01320-7

Figure Lengend Snippet: Fig. 7 A schematic illustration of M1 macrophage-derived CXCL11 in BLM-induced PF in mice. M1 macrophage-derived CXCL11 to modulate M1 macrophage polarization for reverting the fibrogenic process in mice with PF

Article Snippet: For recombinant human CXCL11 (R&D SYSTEMS, Minneapolis, Minnesota, USA) treatment, the mice with fibrosis induction received an IV injection of CXCL11 (2 μg/mouse) on days 10, 12, 13, and 15 after BLM administration.

Techniques: Derivative Assay