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elisa quantikine human il 8 immunoassay kit  (R&D Systems)


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    R&D Systems elisa quantikine human il 8 immunoassay kit
    Elisa Quantikine Human Il 8 Immunoassay Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 632 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 96 stars, based on 632 article reviews
    elisa quantikine human il 8 immunoassay kit - by Bioz Stars, 2026-03
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    SHP2 facilitates the <t>CXCL8</t> secretion of EGFR T790M mutant LUAD. A Differentially expressed mRNA in inhibited, over-expressed and parental PC9GR cells in plot of secreted signaling molecule, a subset of 32 significant genes were identified with an FDR of < 0.05. B mRNA expression of CXCL8 and IL-6 genes showed significant diversity among the three groups, while TGF-β1 mRNA was not significantly altered. Meanwhile the correlation analysis implied a significant correlation coefficient of r = 0.9253 between CXCL8 and SHP2, the relationship of IL-6 and SHP2 was conferred a r = 0.8501. For NGS data analysis, three replicates for each biological group were included in the analysis. C The concentration of CXCL8 in the culture medium of SHP2 over-expressing PC9GRcells was significantly higher than that of parental cells, while the CXCL8 in the supernatant of SHP2 inhibited PC9GR cells was significantly reduced. D Activated ERK, AKT and RelA/p65 were significantly up-regulated in SHP2 over-expressing cells than parental cells, and down-regulated in SHP2 knock-down cells. Each experiment was repeated 3 times
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    Fig. 1. Serum (A) IL6 and (B) <t>IL8</t> concentrations grouped by metastasis location. Data are represented as box plots displaying medians, 25th and 75th percentiles as boxes, and the standard deviation (SD) of the values as whiskers.
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    Aspirin treatment of platelets inhibits tumor cell IL-8 and invasion. Platelets were pretreated with 100 μM aspirin (ASA) or vehicle control for 1 hour, washed to remove residual aspirin, and then activated with TRAP (5 μM) or breast tumor cells (3 × 106/mL). (A) Platelet activation status was determined by <t>p-selectin</t> staining, using flow cytometry. (B) MDA-MB-231 tumor cells were treated with aspirin-treated platelets, lysed, run on an Akt signaling array, and compared with array results from Figure 4A. (C) MDA-MB-231 or MCF-7 cells were exposed to releasates from aspirin-treated or control platelets, and IL-8 release from tumor cells was measured by ELISA at 24 hours. The effect of aspirin pretreatment on the metastatic potential of APR was tested using transwell invasion assays. In addition, 1 ng/mL rhIL-8 was added to TRAP-activated releasates from aspirin-treated platelets. Representative 10× images are shown in panel D, and quantification of MDA-MB-231 invasion is shown in panel E. One value for TRAP-APR was considered an outlier (17.2-fold, with standard deviation from the mean >2.5) and removed from graphical representation and statistical analysis. P values were determined by unpaired Student t tests. n = 3 to 7 independent replicates per treatment group, with the exception of the Akt signaling array, which represents a single experiment. Scale bars represent 100 μm. The dashed black line represents invasion on incubation with resting platelet releasate.
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    R&D Systems quantikine human il 8 immunoassay kit
    Aspirin treatment of platelets inhibits tumor cell IL-8 and invasion. Platelets were pretreated with 100 μM aspirin (ASA) or vehicle control for 1 hour, washed to remove residual aspirin, and then activated with TRAP (5 μM) or breast tumor cells (3 × 106/mL). (A) Platelet activation status was determined by <t>p-selectin</t> staining, using flow cytometry. (B) MDA-MB-231 tumor cells were treated with aspirin-treated platelets, lysed, run on an Akt signaling array, and compared with array results from Figure 4A. (C) MDA-MB-231 or MCF-7 cells were exposed to releasates from aspirin-treated or control platelets, and IL-8 release from tumor cells was measured by ELISA at 24 hours. The effect of aspirin pretreatment on the metastatic potential of APR was tested using transwell invasion assays. In addition, 1 ng/mL rhIL-8 was added to TRAP-activated releasates from aspirin-treated platelets. Representative 10× images are shown in panel D, and quantification of MDA-MB-231 invasion is shown in panel E. One value for TRAP-APR was considered an outlier (17.2-fold, with standard deviation from the mean >2.5) and removed from graphical representation and statistical analysis. P values were determined by unpaired Student t tests. n = 3 to 7 independent replicates per treatment group, with the exception of the Akt signaling array, which represents a single experiment. Scale bars represent 100 μm. The dashed black line represents invasion on incubation with resting platelet releasate.
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    Image Search Results


    Journal: iScience

    Article Title: Establishment of an ulcerative colitis model using colon organoids derived from human induced pluripotent stem cells

    doi: 10.1016/j.isci.2024.111049

    Figure Lengend Snippet:

    Article Snippet: IL-8 concentrations in the culture supernatants of hiPSC-COs were measured using Quantikine® ELISA Human IL 8/CXCL8 Immunoassay (Cat# D8000C, R&D Systems).

    Techniques: Recombinant, Membrane, Modification, SYBR Green Assay, Saline, Blocking Assay, Staining, Protease Inhibitor, CCK-8 Assay, Enzyme-linked Immunosorbent Assay, Cytotoxicity Assay, Software, Simple Western, Real-time Polymerase Chain Reaction

    SHP2 facilitates the CXCL8 secretion of EGFR T790M mutant LUAD. A Differentially expressed mRNA in inhibited, over-expressed and parental PC9GR cells in plot of secreted signaling molecule, a subset of 32 significant genes were identified with an FDR of < 0.05. B mRNA expression of CXCL8 and IL-6 genes showed significant diversity among the three groups, while TGF-β1 mRNA was not significantly altered. Meanwhile the correlation analysis implied a significant correlation coefficient of r = 0.9253 between CXCL8 and SHP2, the relationship of IL-6 and SHP2 was conferred a r = 0.8501. For NGS data analysis, three replicates for each biological group were included in the analysis. C The concentration of CXCL8 in the culture medium of SHP2 over-expressing PC9GRcells was significantly higher than that of parental cells, while the CXCL8 in the supernatant of SHP2 inhibited PC9GR cells was significantly reduced. D Activated ERK, AKT and RelA/p65 were significantly up-regulated in SHP2 over-expressing cells than parental cells, and down-regulated in SHP2 knock-down cells. Each experiment was repeated 3 times

    Journal: Cancer Cell International

    Article Title: SHP2 inhibition enhances the anticancer effect of Osimertinib in EGFR T790M mutant lung adenocarcinoma by blocking CXCL8 loop mediated stemness

    doi: 10.1186/s12935-021-02056-x

    Figure Lengend Snippet: SHP2 facilitates the CXCL8 secretion of EGFR T790M mutant LUAD. A Differentially expressed mRNA in inhibited, over-expressed and parental PC9GR cells in plot of secreted signaling molecule, a subset of 32 significant genes were identified with an FDR of < 0.05. B mRNA expression of CXCL8 and IL-6 genes showed significant diversity among the three groups, while TGF-β1 mRNA was not significantly altered. Meanwhile the correlation analysis implied a significant correlation coefficient of r = 0.9253 between CXCL8 and SHP2, the relationship of IL-6 and SHP2 was conferred a r = 0.8501. For NGS data analysis, three replicates for each biological group were included in the analysis. C The concentration of CXCL8 in the culture medium of SHP2 over-expressing PC9GRcells was significantly higher than that of parental cells, while the CXCL8 in the supernatant of SHP2 inhibited PC9GR cells was significantly reduced. D Activated ERK, AKT and RelA/p65 were significantly up-regulated in SHP2 over-expressing cells than parental cells, and down-regulated in SHP2 knock-down cells. Each experiment was repeated 3 times

    Article Snippet: Human CXCL8 Immunoassay Quantikine ELISA Kit (Cat#:D8000C) was purchased from R&D Systems.

    Techniques: Mutagenesis, Expressing, Concentration Assay, Knockdown

    SHP2 inhibition suppresses the stemness and tumorigenesis of EGFR T790M mutant LUAD by CXCL8/CXCR1 positive feedback loop. A The clones were dramatically inhibited by Danirixin or Reparixin, while exogenous CXCL8 significantly enhanced the colony formation of PC9GR. B The percentage of CSCs was reduced in the setting of CXCL8-CXCR1/2 loop blockage, and recombinant CXCL8 could reverse the CSCs proportion. C In SHP2 over-expressed panel, Danirixin and Reparixin respectively decreased the CSCs to 6.193 ± 0.875 % and 5.703 ± 0.419 % from 11.223 ± 0.738 %, however additional CXCL8 raised the CSCs to 14.040 ± 0.397 %. In SHP2 inhibited panel, Danirixin and Reparixin respectively decreased the CSCs to 1.807 ± 0.309 % and 1.970 ± 0.471 % from 3.757 ± 0.237 %, but additional CXCL8 increased the CSCs to 7.010 ± 0.920 %. D CXCL8-CXCR1/2 blockage limits the weight of SHP2 high PC9GR tumors than that of treated with DMSO, which decreased from 2.050 ± 0.184 g to 0.850 ± 0.023 g and 0.993 ± 0.070 g, and tumor weight SHP2 inhibited cells reduced from 1.576 ± 0.116 g to 0.510 ± 0.106 g and 0.474 ± 0.055 g, respectively. Each experiment was repeated 3 times

    Journal: Cancer Cell International

    Article Title: SHP2 inhibition enhances the anticancer effect of Osimertinib in EGFR T790M mutant lung adenocarcinoma by blocking CXCL8 loop mediated stemness

    doi: 10.1186/s12935-021-02056-x

    Figure Lengend Snippet: SHP2 inhibition suppresses the stemness and tumorigenesis of EGFR T790M mutant LUAD by CXCL8/CXCR1 positive feedback loop. A The clones were dramatically inhibited by Danirixin or Reparixin, while exogenous CXCL8 significantly enhanced the colony formation of PC9GR. B The percentage of CSCs was reduced in the setting of CXCL8-CXCR1/2 loop blockage, and recombinant CXCL8 could reverse the CSCs proportion. C In SHP2 over-expressed panel, Danirixin and Reparixin respectively decreased the CSCs to 6.193 ± 0.875 % and 5.703 ± 0.419 % from 11.223 ± 0.738 %, however additional CXCL8 raised the CSCs to 14.040 ± 0.397 %. In SHP2 inhibited panel, Danirixin and Reparixin respectively decreased the CSCs to 1.807 ± 0.309 % and 1.970 ± 0.471 % from 3.757 ± 0.237 %, but additional CXCL8 increased the CSCs to 7.010 ± 0.920 %. D CXCL8-CXCR1/2 blockage limits the weight of SHP2 high PC9GR tumors than that of treated with DMSO, which decreased from 2.050 ± 0.184 g to 0.850 ± 0.023 g and 0.993 ± 0.070 g, and tumor weight SHP2 inhibited cells reduced from 1.576 ± 0.116 g to 0.510 ± 0.106 g and 0.474 ± 0.055 g, respectively. Each experiment was repeated 3 times

    Article Snippet: Human CXCL8 Immunoassay Quantikine ELISA Kit (Cat#:D8000C) was purchased from R&D Systems.

    Techniques: Inhibition, Mutagenesis, Clone Assay, Recombinant

    The role of SHP2 derived CXCL8/CXCR1 positive feedback loop in EGFR T790M mutant LUAD

    Journal: Cancer Cell International

    Article Title: SHP2 inhibition enhances the anticancer effect of Osimertinib in EGFR T790M mutant lung adenocarcinoma by blocking CXCL8 loop mediated stemness

    doi: 10.1186/s12935-021-02056-x

    Figure Lengend Snippet: The role of SHP2 derived CXCL8/CXCR1 positive feedback loop in EGFR T790M mutant LUAD

    Article Snippet: Human CXCL8 Immunoassay Quantikine ELISA Kit (Cat#:D8000C) was purchased from R&D Systems.

    Techniques: Derivative Assay, Mutagenesis

    Fig. 1. Serum (A) IL6 and (B) IL8 concentrations grouped by metastasis location. Data are represented as box plots displaying medians, 25th and 75th percentiles as boxes, and the standard deviation (SD) of the values as whiskers.

    Journal: Cytokine

    Article Title: Interleukin-6 and interleukin-8 serum levels in prognosis of hormone-dependent breast cancer.

    doi: 10.1016/j.cyto.2018.02.019

    Figure Lengend Snippet: Fig. 1. Serum (A) IL6 and (B) IL8 concentrations grouped by metastasis location. Data are represented as box plots displaying medians, 25th and 75th percentiles as boxes, and the standard deviation (SD) of the values as whiskers.

    Article Snippet: IL6 and IL8 levels were determined by ELISA from serum samples according to the manufacturer’s instructions (Quantikine Human IL6 and Quantikine Human IL8 Immunoassay kits, R&D Systems, Minneapolis, MN).

    Techniques: Standard Deviation

    Fig. 2. Kaplan-Meier prognostic analysis of IL6 and IL8 in the entire patient group. Plots represent (A), serum IL6 levels over the entire patient group (B), serum IL8 levels over the entire patient group (C), serum IL8 levels in the ERhigh subgroup (D), serum IL8 levels in the HER2+ subgroup. Upper and lower curves represent the IL6high/IL6low or IL8high/ IL8low patient subgroups defined by an optimal outcome-oriented cutoff. The exact cutoff values are indicated for each plot. Patients with higher cytokine values above the cutoff are plotted on solid lines, while lower values are presented on dotted lines. A wider separation between upper and lower curves indicates better prognostic performance. P- values were calculated by the Cox proportional hazards regression test. Metastasis in- cidences in patient subgroups prognosticated as low- and high-risk were respectively: (A) 0/27%, (B) 16/33%, (C) 14/35% and (D) 0/44%. Metastasis-free survival time in months is indicated on the x-axis.

    Journal: Cytokine

    Article Title: Interleukin-6 and interleukin-8 serum levels in prognosis of hormone-dependent breast cancer.

    doi: 10.1016/j.cyto.2018.02.019

    Figure Lengend Snippet: Fig. 2. Kaplan-Meier prognostic analysis of IL6 and IL8 in the entire patient group. Plots represent (A), serum IL6 levels over the entire patient group (B), serum IL8 levels over the entire patient group (C), serum IL8 levels in the ERhigh subgroup (D), serum IL8 levels in the HER2+ subgroup. Upper and lower curves represent the IL6high/IL6low or IL8high/ IL8low patient subgroups defined by an optimal outcome-oriented cutoff. The exact cutoff values are indicated for each plot. Patients with higher cytokine values above the cutoff are plotted on solid lines, while lower values are presented on dotted lines. A wider separation between upper and lower curves indicates better prognostic performance. P- values were calculated by the Cox proportional hazards regression test. Metastasis in- cidences in patient subgroups prognosticated as low- and high-risk were respectively: (A) 0/27%, (B) 16/33%, (C) 14/35% and (D) 0/44%. Metastasis-free survival time in months is indicated on the x-axis.

    Article Snippet: IL6 and IL8 levels were determined by ELISA from serum samples according to the manufacturer’s instructions (Quantikine Human IL6 and Quantikine Human IL8 Immunoassay kits, R&D Systems, Minneapolis, MN).

    Techniques:

    Aspirin treatment of platelets inhibits tumor cell IL-8 and invasion. Platelets were pretreated with 100 μM aspirin (ASA) or vehicle control for 1 hour, washed to remove residual aspirin, and then activated with TRAP (5 μM) or breast tumor cells (3 × 106/mL). (A) Platelet activation status was determined by p-selectin staining, using flow cytometry. (B) MDA-MB-231 tumor cells were treated with aspirin-treated platelets, lysed, run on an Akt signaling array, and compared with array results from Figure 4A. (C) MDA-MB-231 or MCF-7 cells were exposed to releasates from aspirin-treated or control platelets, and IL-8 release from tumor cells was measured by ELISA at 24 hours. The effect of aspirin pretreatment on the metastatic potential of APR was tested using transwell invasion assays. In addition, 1 ng/mL rhIL-8 was added to TRAP-activated releasates from aspirin-treated platelets. Representative 10× images are shown in panel D, and quantification of MDA-MB-231 invasion is shown in panel E. One value for TRAP-APR was considered an outlier (17.2-fold, with standard deviation from the mean >2.5) and removed from graphical representation and statistical analysis. P values were determined by unpaired Student t tests. n = 3 to 7 independent replicates per treatment group, with the exception of the Akt signaling array, which represents a single experiment. Scale bars represent 100 μm. The dashed black line represents invasion on incubation with resting platelet releasate.

    Journal: Blood Advances

    Article Title: Aspirin inhibits platelets from reprogramming breast tumor cells and promoting metastasis

    doi: 10.1182/bloodadvances.2018026161

    Figure Lengend Snippet: Aspirin treatment of platelets inhibits tumor cell IL-8 and invasion. Platelets were pretreated with 100 μM aspirin (ASA) or vehicle control for 1 hour, washed to remove residual aspirin, and then activated with TRAP (5 μM) or breast tumor cells (3 × 106/mL). (A) Platelet activation status was determined by p-selectin staining, using flow cytometry. (B) MDA-MB-231 tumor cells were treated with aspirin-treated platelets, lysed, run on an Akt signaling array, and compared with array results from Figure 4A. (C) MDA-MB-231 or MCF-7 cells were exposed to releasates from aspirin-treated or control platelets, and IL-8 release from tumor cells was measured by ELISA at 24 hours. The effect of aspirin pretreatment on the metastatic potential of APR was tested using transwell invasion assays. In addition, 1 ng/mL rhIL-8 was added to TRAP-activated releasates from aspirin-treated platelets. Representative 10× images are shown in panel D, and quantification of MDA-MB-231 invasion is shown in panel E. One value for TRAP-APR was considered an outlier (17.2-fold, with standard deviation from the mean >2.5) and removed from graphical representation and statistical analysis. P values were determined by unpaired Student t tests. n = 3 to 7 independent replicates per treatment group, with the exception of the Akt signaling array, which represents a single experiment. Scale bars represent 100 μm. The dashed black line represents invasion on incubation with resting platelet releasate.

    Article Snippet: Quantikine Human IL-8, RANTES (CCL5) and p -selectin Immunoassays (R&D Systems, Minneapolis, MN; catalog no.: D8000C, DRN00B, and BBE6, respectively) were used according to the manufacturer’s instructions on patient serum, run in duplicate.

    Techniques: Control, Activation Assay, Staining, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Standard Deviation, Incubation

    Patients with breast cancer receiving aspirin have decreased plasma IL-8 levels and platelets with impaired metastatic potential. (A) Tumor tissue from aspirin-treated or non-aspirin–treated (control) mice bearing MCF-7ras tumors was collected and stained for human IL-8 by immunohistochemistry. Tumors from 5 separate 100 mg/kg aspirin-treated mice and 5 control mice are shown, and semiquantitative analysis performed based on optical density. Platelets and plasma were isolated from patients with breast cancer (BC) who were either taking or not taking aspirin (81-325 mg/d). Plasma levels of soluble p-selectin (B), CCL5 (C), and IL-8 (D) were then measured by ELISA. Platelets isolated from patients were exposed to MDA-MB-231 breast tumor cells; APR was collected and used for the following: APR CCL5 measured by ELISA (E), APR was used to treat MDA-MB-231 cells for 24 hours and IL-8 secretion was measured by ELISA (F), and APR was used in Matrigel invasion assays with MDA-MB-231 cells (G-H). Scale bars represent 100 μm. P values were obtained through separate 1-way ANOVA, with post hoc Tukey’s multiple comparisons testing. n = 7 to 9 independent replicates per treatment group in panels B-D and 3 to 6 independent replicates per treatment group in panels E-F and H.

    Journal: Blood Advances

    Article Title: Aspirin inhibits platelets from reprogramming breast tumor cells and promoting metastasis

    doi: 10.1182/bloodadvances.2018026161

    Figure Lengend Snippet: Patients with breast cancer receiving aspirin have decreased plasma IL-8 levels and platelets with impaired metastatic potential. (A) Tumor tissue from aspirin-treated or non-aspirin–treated (control) mice bearing MCF-7ras tumors was collected and stained for human IL-8 by immunohistochemistry. Tumors from 5 separate 100 mg/kg aspirin-treated mice and 5 control mice are shown, and semiquantitative analysis performed based on optical density. Platelets and plasma were isolated from patients with breast cancer (BC) who were either taking or not taking aspirin (81-325 mg/d). Plasma levels of soluble p-selectin (B), CCL5 (C), and IL-8 (D) were then measured by ELISA. Platelets isolated from patients were exposed to MDA-MB-231 breast tumor cells; APR was collected and used for the following: APR CCL5 measured by ELISA (E), APR was used to treat MDA-MB-231 cells for 24 hours and IL-8 secretion was measured by ELISA (F), and APR was used in Matrigel invasion assays with MDA-MB-231 cells (G-H). Scale bars represent 100 μm. P values were obtained through separate 1-way ANOVA, with post hoc Tukey’s multiple comparisons testing. n = 7 to 9 independent replicates per treatment group in panels B-D and 3 to 6 independent replicates per treatment group in panels E-F and H.

    Article Snippet: Quantikine Human IL-8, RANTES (CCL5) and p -selectin Immunoassays (R&D Systems, Minneapolis, MN; catalog no.: D8000C, DRN00B, and BBE6, respectively) were used according to the manufacturer’s instructions on patient serum, run in duplicate.

    Techniques: Clinical Proteomics, Control, Staining, Immunohistochemistry, Isolation, Enzyme-linked Immunosorbent Assay