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enzyme linked immunosorbent assay elisa kit  (R&D Systems)


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    R&D Systems enzyme linked immunosorbent assay elisa kit
    Enzyme Linked Immunosorbent Assay Elisa Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 195 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ip+10+elisa+kit/Mouse+CXCL10%2FIP-10%2FCRG-2+DuoSet+ELISA/pm42018138-109-20-25
    Average 96 stars, based on 195 article reviews
    enzyme linked immunosorbent assay elisa kit - by Bioz Stars, 2026-10
    96/100 stars

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    Enzyme-linked Immunosorbent Assay:

    Article Title: Reduced intestinal GLP-1 + cell numbers are associated with an inflammation-related epithelial metabolic signature
    Article Snippet: .. IP-10 concentrations were determined using an IP-10 ELISA kit (R&D Systems) according to the manufacturer’s instructions. .. Life- and dead- cell protease activity was measured using the MultiTox-Fluor Cytotoxicity Assay and ATP content was determined using the CellTiter-Glo Luminescent Cell Viability Assay (both from Promega), according to the manufacturer’s instructions.

    Article Title: Urine IP-10 as a biomarker of therapeutic response in patients with active pulmonary tuberculosis.
    Article Snippet: .. IP-10 levels in urine and serum were concomitantly measured in duplicate using a commercial IP-10 ELISA Kit (R&D Systems, Minneapolis, MN, USA) in accordance with the manufacturer’s instructions. .. The test results were interpreted using SoftMax version 5.4.1 (Molecular Devices, LLC, Sunnyvale, CA, USA).

    Article Title: Reduced Intestinal GLP-1 + Cell Numbers Are Associated With an Inflammation-related Epithelial Metabolic Signature
    Article Snippet: .. IP-10 concentrations were determined using an IP-10 ELISA kit (R&D Systems) according to the manufacturer’s instructions. .. Life- and dead- cell protease activity was measured using the MultiTox-Fluor Cytotoxicity Assay, and ATP content was determined using the CellTiter-Glo Luminescent Cell Viability Assay (both from Promega), according to the manufacturer’s instructions.

    Article Title: The Roles of Chemokines in Rabies Virus Infection: Overexpression May Not Always Be Beneficial
    Article Snippet: .. The supernatant was subjected to an enzyme-linked immunosorbent assay (ELISA) to quantify the amount of MIP-1 , RANTES, and IP-10 individually in cell culture supernatants or mouse brain suspensions by using the murine MIP-1 , RANTES, and IP-10 ELISA kit (R&D Systems, Minneapolis, MN) according to the manufacturer’s protocol. .. A multiplex ELISA kit (Quansys Biosciences, Logan, UT) was used to quantify a panel of 16 cytokines (interleukin-1 [IL-1 ], IL-1 , IL-2, IL-3, IL-4, IL-5, IL-6, IL-10, IL-12p70, IL-17, MCP-1, IFN- , tumor necrosis factor alpha [TNF- ], MIP-1 , granulocyte-macrophage colony-stimulating factor, and RANTES) in brain extracts according to the manufacturer’s protocol.

    Cell Culture:

    Article Title: The Roles of Chemokines in Rabies Virus Infection: Overexpression May Not Always Be Beneficial
    Article Snippet: .. The supernatant was subjected to an enzyme-linked immunosorbent assay (ELISA) to quantify the amount of MIP-1 , RANTES, and IP-10 individually in cell culture supernatants or mouse brain suspensions by using the murine MIP-1 , RANTES, and IP-10 ELISA kit (R&D Systems, Minneapolis, MN) according to the manufacturer’s protocol. .. A multiplex ELISA kit (Quansys Biosciences, Logan, UT) was used to quantify a panel of 16 cytokines (interleukin-1 [IL-1 ], IL-1 , IL-2, IL-3, IL-4, IL-5, IL-6, IL-10, IL-12p70, IL-17, MCP-1, IFN- , tumor necrosis factor alpha [TNF- ], MIP-1 , granulocyte-macrophage colony-stimulating factor, and RANTES) in brain extracts according to the manufacturer’s protocol.



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    CXCL10 is upregulated in both macrophages and fibroblasts responding to aged ZnO NPs exposure. (A) Heatmaps exhibited multiplex cytokine profiling of serum and BALF from IT (PBS/fresh NPs/aged NPs intratracheal instillation) and IT + IV (IT exposure followed by intravenous injection of 4T1 cells) models ( n = 3). (B–E) Concentrations of significantly dyregulated cytokines in serum and BALF from mice exposed to ZnO NPs (fresh or aged), with or without subsequent 4T1 cell injection ( n = 3). (F) Venn plot showed the overlapping cytokines in serum and BALF between IT and IT + IV models. (G) <t>ELISA</t> detection of CXCL10 concentrations in serum and BALF of IT and IT + IV groups ( n = 3). (H) qPCR analysis of CXCL10 mRNA in lung tissue, primary fibroblasts, and alveolar macrophages post‐IT, normalized to GAPDH ( n = 3). (I, J) UMAP visualization (I) and dot plot (J) displaying CXCL10 expression across annotated cell types. (K, L) UMAP visualization (K) and dot plot (L) displaying CXCL10 expression across myeloid cell types. (M) Representative images of invasion and migration assays of 4T1 cells stimulated with 50 or 100 ng/mL murine recombinant CXCL10 (rCXCL10) for 72 h ( n = 3). (N) Quantification of invasion and migration assays ( n = 3). All data were represented as the mean ± SD. P values were calculated by one‐way ANOVA followed by Tukey's test. * p < 0.05, ** p < 0.01 vs control group; # p < 0.05, ## p < 0.01 vs fresh NPs group.
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    CXCL10 is upregulated in both macrophages and fibroblasts responding to aged ZnO NPs exposure. (A) Heatmaps exhibited multiplex cytokine profiling of serum and BALF from IT (PBS/fresh NPs/aged NPs intratracheal instillation) and IT + IV (IT exposure followed by intravenous injection of 4T1 cells) models ( n = 3). (B–E) Concentrations of significantly dyregulated cytokines in serum and BALF from mice exposed to ZnO NPs (fresh or aged), with or without subsequent 4T1 cell injection ( n = 3). (F) Venn plot showed the overlapping cytokines in serum and BALF between IT and IT + IV models. (G) <t>ELISA</t> detection of CXCL10 concentrations in serum and BALF of IT and IT + IV groups ( n = 3). (H) qPCR analysis of CXCL10 mRNA in lung tissue, primary fibroblasts, and alveolar macrophages post‐IT, normalized to GAPDH ( n = 3). (I, J) UMAP visualization (I) and dot plot (J) displaying CXCL10 expression across annotated cell types. (K, L) UMAP visualization (K) and dot plot (L) displaying CXCL10 expression across myeloid cell types. (M) Representative images of invasion and migration assays of 4T1 cells stimulated with 50 or 100 ng/mL murine recombinant CXCL10 (rCXCL10) for 72 h ( n = 3). (N) Quantification of invasion and migration assays ( n = 3). All data were represented as the mean ± SD. P values were calculated by one‐way ANOVA followed by Tukey's test. * p < 0.05, ** p < 0.01 vs control group; # p < 0.05, ## p < 0.01 vs fresh NPs group.
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    CXCL10 is upregulated in both macrophages and fibroblasts responding to aged ZnO NPs exposure. (A) Heatmaps exhibited multiplex cytokine profiling of serum and BALF from IT (PBS/fresh NPs/aged NPs intratracheal instillation) and IT + IV (IT exposure followed by intravenous injection of 4T1 cells) models ( n = 3). (B–E) Concentrations of significantly dyregulated cytokines in serum and BALF from mice exposed to ZnO NPs (fresh or aged), with or without subsequent 4T1 cell injection ( n = 3). (F) Venn plot showed the overlapping cytokines in serum and BALF between IT and IT + IV models. (G) <t>ELISA</t> detection of CXCL10 concentrations in serum and BALF of IT and IT + IV groups ( n = 3). (H) qPCR analysis of CXCL10 mRNA in lung tissue, primary fibroblasts, and alveolar macrophages post‐IT, normalized to GAPDH ( n = 3). (I, J) UMAP visualization (I) and dot plot (J) displaying CXCL10 expression across annotated cell types. (K, L) UMAP visualization (K) and dot plot (L) displaying CXCL10 expression across myeloid cell types. (M) Representative images of invasion and migration assays of 4T1 cells stimulated with 50 or 100 ng/mL murine recombinant CXCL10 (rCXCL10) for 72 h ( n = 3). (N) Quantification of invasion and migration assays ( n = 3). All data were represented as the mean ± SD. P values were calculated by one‐way ANOVA followed by Tukey's test. * p < 0.05, ** p < 0.01 vs control group; # p < 0.05, ## p < 0.01 vs fresh NPs group.
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    G9a inhibition potentiates the immunogenic effects of IFN-γ in HCC cells (A) Effect of CM272 and EZM8266 on IFN-γ-triggered <t>CXCL10</t> production in murine (PM299L) and human (HuH7) HCC cells. Cells were treated with CM272 for 48 h or with CM272 for 24 h and then with IFN-γ (75 U/mL) for another 24 h or with IFN-γ alone for 24 h. PM299L were treated with 400 nM, and HuH7 received 1 μM of CM272 ( n = 3). For EZM8266, cells were pretreated for 48 h with EZM8266 (5 mM) and then with IFN-γ (75 U/mL) for another 24 h, as indicated. CXCL10 protein levels were measured by ELISA in cells’ conditioned media ( n = 3). (B) Effect of G9a inhibition with CM272 or EZM8266 on the expression of MHC class I complex protein (MHC-I) on the surface of PM299L cells. Cells were treated with IFN-γ and CM272 or EZM8266 as indicated in (A), and MHC-I levels were determined by FACS analysis ( n = 3). (C) ChIP analyses of H3K9me2 levels in the proximal promoter regions of CXCL10 and HLA-A genes in HuH7 cells treated with IFN-γ (75 U/mL) and CM272 (400 nM), as indicated in (A) ( n = 3). (D) Evaluation of the expression of transposable elements (TEs) and endogenous retroviral sequences (ERVs) by RNA-seq in NM53 murine HCC cells treated with IFN-γ, CM272, and their combination as indicated in (A). (E) Immunofluorescence analyses of dsRNA in PM299L HCC cells treated with CM272 (24 h) or EZM8266 (48 h). Representative images are shown. Scale bars, 10 μm. Right panel shows a control without primary antibody ( n = 3). Data are represented as mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. All the replicates represent biological replicates.
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    G9a inhibition potentiates the immunogenic effects of IFN-γ in HCC cells (A) Effect of CM272 and EZM8266 on IFN-γ-triggered <t>CXCL10</t> production in murine (PM299L) and human (HuH7) HCC cells. Cells were treated with CM272 for 48 h or with CM272 for 24 h and then with IFN-γ (75 U/mL) for another 24 h or with IFN-γ alone for 24 h. PM299L were treated with 400 nM, and HuH7 received 1 μM of CM272 ( n = 3). For EZM8266, cells were pretreated for 48 h with EZM8266 (5 mM) and then with IFN-γ (75 U/mL) for another 24 h, as indicated. CXCL10 protein levels were measured by ELISA in cells’ conditioned media ( n = 3). (B) Effect of G9a inhibition with CM272 or EZM8266 on the expression of MHC class I complex protein (MHC-I) on the surface of PM299L cells. Cells were treated with IFN-γ and CM272 or EZM8266 as indicated in (A), and MHC-I levels were determined by FACS analysis ( n = 3). (C) ChIP analyses of H3K9me2 levels in the proximal promoter regions of CXCL10 and HLA-A genes in HuH7 cells treated with IFN-γ (75 U/mL) and CM272 (400 nM), as indicated in (A) ( n = 3). (D) Evaluation of the expression of transposable elements (TEs) and endogenous retroviral sequences (ERVs) by RNA-seq in NM53 murine HCC cells treated with IFN-γ, CM272, and their combination as indicated in (A). (E) Immunofluorescence analyses of dsRNA in PM299L HCC cells treated with CM272 (24 h) or EZM8266 (48 h). Representative images are shown. Scale bars, 10 μm. Right panel shows a control without primary antibody ( n = 3). Data are represented as mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. All the replicates represent biological replicates.
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    Image Search Results


    CXCL10 is upregulated in both macrophages and fibroblasts responding to aged ZnO NPs exposure. (A) Heatmaps exhibited multiplex cytokine profiling of serum and BALF from IT (PBS/fresh NPs/aged NPs intratracheal instillation) and IT + IV (IT exposure followed by intravenous injection of 4T1 cells) models ( n = 3). (B–E) Concentrations of significantly dyregulated cytokines in serum and BALF from mice exposed to ZnO NPs (fresh or aged), with or without subsequent 4T1 cell injection ( n = 3). (F) Venn plot showed the overlapping cytokines in serum and BALF between IT and IT + IV models. (G) ELISA detection of CXCL10 concentrations in serum and BALF of IT and IT + IV groups ( n = 3). (H) qPCR analysis of CXCL10 mRNA in lung tissue, primary fibroblasts, and alveolar macrophages post‐IT, normalized to GAPDH ( n = 3). (I, J) UMAP visualization (I) and dot plot (J) displaying CXCL10 expression across annotated cell types. (K, L) UMAP visualization (K) and dot plot (L) displaying CXCL10 expression across myeloid cell types. (M) Representative images of invasion and migration assays of 4T1 cells stimulated with 50 or 100 ng/mL murine recombinant CXCL10 (rCXCL10) for 72 h ( n = 3). (N) Quantification of invasion and migration assays ( n = 3). All data were represented as the mean ± SD. P values were calculated by one‐way ANOVA followed by Tukey's test. * p < 0.05, ** p < 0.01 vs control group; # p < 0.05, ## p < 0.01 vs fresh NPs group.

    Journal: Advanced Science

    Article Title: Aged ZnO Nanoparticles Promote Breast Cancer Lung Metastasis by Remodeling the Pulmonary Microenvironment Through the CXCL10/Wnt/β‐Catenin Axis

    doi: 10.1002/advs.78249

    Figure Lengend Snippet: CXCL10 is upregulated in both macrophages and fibroblasts responding to aged ZnO NPs exposure. (A) Heatmaps exhibited multiplex cytokine profiling of serum and BALF from IT (PBS/fresh NPs/aged NPs intratracheal instillation) and IT + IV (IT exposure followed by intravenous injection of 4T1 cells) models ( n = 3). (B–E) Concentrations of significantly dyregulated cytokines in serum and BALF from mice exposed to ZnO NPs (fresh or aged), with or without subsequent 4T1 cell injection ( n = 3). (F) Venn plot showed the overlapping cytokines in serum and BALF between IT and IT + IV models. (G) ELISA detection of CXCL10 concentrations in serum and BALF of IT and IT + IV groups ( n = 3). (H) qPCR analysis of CXCL10 mRNA in lung tissue, primary fibroblasts, and alveolar macrophages post‐IT, normalized to GAPDH ( n = 3). (I, J) UMAP visualization (I) and dot plot (J) displaying CXCL10 expression across annotated cell types. (K, L) UMAP visualization (K) and dot plot (L) displaying CXCL10 expression across myeloid cell types. (M) Representative images of invasion and migration assays of 4T1 cells stimulated with 50 or 100 ng/mL murine recombinant CXCL10 (rCXCL10) for 72 h ( n = 3). (N) Quantification of invasion and migration assays ( n = 3). All data were represented as the mean ± SD. P values were calculated by one‐way ANOVA followed by Tukey's test. * p < 0.05, ** p < 0.01 vs control group; # p < 0.05, ## p < 0.01 vs fresh NPs group.

    Article Snippet: CXCL10 (IP‐10) levels were measured using a mouse ELISA kit (Elabscience, E‐EL‐M0021) following the manufacturer's instructions.

    Techniques: Multiplex Assay, Profiling, Injection, Enzyme-linked Immunosorbent Assay, Analysis, Tissue, Expressing, Migration, Recombinant, Control

    G9a inhibition potentiates the immunogenic effects of IFN-γ in HCC cells (A) Effect of CM272 and EZM8266 on IFN-γ-triggered CXCL10 production in murine (PM299L) and human (HuH7) HCC cells. Cells were treated with CM272 for 48 h or with CM272 for 24 h and then with IFN-γ (75 U/mL) for another 24 h or with IFN-γ alone for 24 h. PM299L were treated with 400 nM, and HuH7 received 1 μM of CM272 ( n = 3). For EZM8266, cells were pretreated for 48 h with EZM8266 (5 mM) and then with IFN-γ (75 U/mL) for another 24 h, as indicated. CXCL10 protein levels were measured by ELISA in cells’ conditioned media ( n = 3). (B) Effect of G9a inhibition with CM272 or EZM8266 on the expression of MHC class I complex protein (MHC-I) on the surface of PM299L cells. Cells were treated with IFN-γ and CM272 or EZM8266 as indicated in (A), and MHC-I levels were determined by FACS analysis ( n = 3). (C) ChIP analyses of H3K9me2 levels in the proximal promoter regions of CXCL10 and HLA-A genes in HuH7 cells treated with IFN-γ (75 U/mL) and CM272 (400 nM), as indicated in (A) ( n = 3). (D) Evaluation of the expression of transposable elements (TEs) and endogenous retroviral sequences (ERVs) by RNA-seq in NM53 murine HCC cells treated with IFN-γ, CM272, and their combination as indicated in (A). (E) Immunofluorescence analyses of dsRNA in PM299L HCC cells treated with CM272 (24 h) or EZM8266 (48 h). Representative images are shown. Scale bars, 10 μm. Right panel shows a control without primary antibody ( n = 3). Data are represented as mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. All the replicates represent biological replicates.

    Journal: Cell Reports Medicine

    Article Title: Histone methyl-transferase G9a inhibition boosts the efficacy of immune checkpoint inhibitors in experimental hepatocellular carcinoma

    doi: 10.1016/j.xcrm.2026.102717

    Figure Lengend Snippet: G9a inhibition potentiates the immunogenic effects of IFN-γ in HCC cells (A) Effect of CM272 and EZM8266 on IFN-γ-triggered CXCL10 production in murine (PM299L) and human (HuH7) HCC cells. Cells were treated with CM272 for 48 h or with CM272 for 24 h and then with IFN-γ (75 U/mL) for another 24 h or with IFN-γ alone for 24 h. PM299L were treated with 400 nM, and HuH7 received 1 μM of CM272 ( n = 3). For EZM8266, cells were pretreated for 48 h with EZM8266 (5 mM) and then with IFN-γ (75 U/mL) for another 24 h, as indicated. CXCL10 protein levels were measured by ELISA in cells’ conditioned media ( n = 3). (B) Effect of G9a inhibition with CM272 or EZM8266 on the expression of MHC class I complex protein (MHC-I) on the surface of PM299L cells. Cells were treated with IFN-γ and CM272 or EZM8266 as indicated in (A), and MHC-I levels were determined by FACS analysis ( n = 3). (C) ChIP analyses of H3K9me2 levels in the proximal promoter regions of CXCL10 and HLA-A genes in HuH7 cells treated with IFN-γ (75 U/mL) and CM272 (400 nM), as indicated in (A) ( n = 3). (D) Evaluation of the expression of transposable elements (TEs) and endogenous retroviral sequences (ERVs) by RNA-seq in NM53 murine HCC cells treated with IFN-γ, CM272, and their combination as indicated in (A). (E) Immunofluorescence analyses of dsRNA in PM299L HCC cells treated with CM272 (24 h) or EZM8266 (48 h). Representative images are shown. Scale bars, 10 μm. Right panel shows a control without primary antibody ( n = 3). Data are represented as mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. All the replicates represent biological replicates.

    Article Snippet: CXCL9 and CXCL10 concentrations were measured in culture supernatants collected at the end of the incubation periods using commercial ELISA kits for mouse CXCL9 (DY492) and CXCL10 (DY466), both from R&D Systems, and an ELISA kit for human CXCL10 (550926) from BD Biosciences (Franklin Lanes, NJ, USA).

    Techniques: Inhibition, Enzyme-linked Immunosorbent Assay, Expressing, Retroviral, RNA Sequencing, Immunofluorescence, Control