mouse trem1‐fc Search Results


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    R&D Systems soluble trem 1
    <t>TREM-1</t> deficiency attenuates NOX2-derived superoxide in response to OpZ. Rate (A) and maximal velocity (V max ) (B) of superoxide and hydroxyl radical production in WT, Trem-1/3 −/− , Cybb −/− , and Trem-1/3 −/− /Cybb −/− neutrophils following OpZ stimulation. Data from 3 experiments were compiled and are shown as Mean ± SEM, 3–5 pooled mice/data point. * P
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    TREM-1 deficiency attenuates NOX2-derived superoxide in response to OpZ. Rate (A) and maximal velocity (V max ) (B) of superoxide and hydroxyl radical production in WT, Trem-1/3 −/− , Cybb −/− , and Trem-1/3 −/− /Cybb −/− neutrophils following OpZ stimulation. Data from 3 experiments were compiled and are shown as Mean ± SEM, 3–5 pooled mice/data point. * P

    Journal: Journal of leukocyte biology

    Article Title: TREM-1 regulates neutrophil chemotaxis by promoting NOX-dependent superoxide production

    doi: 10.1002/JLB.3VMA0918-375R

    Figure Lengend Snippet: TREM-1 deficiency attenuates NOX2-derived superoxide in response to OpZ. Rate (A) and maximal velocity (V max ) (B) of superoxide and hydroxyl radical production in WT, Trem-1/3 −/− , Cybb −/− , and Trem-1/3 −/− /Cybb −/− neutrophils following OpZ stimulation. Data from 3 experiments were compiled and are shown as Mean ± SEM, 3–5 pooled mice/data point. * P

    Article Snippet: Genotypes were determined by PCR for both Trem1/3 and Cybb and confirmed by FACs analysis of blood for TREM-1, using anti-mouse TREM-1, clone 174031 (R & D Systems), and dihydrorhodamine (DHR; Thermofisher Scientific) for ROS production with PMA (Sigma) stimulation.

    Techniques: Derivative Assay, Mouse Assay

    TREM-1 deficiency impairs neutrophil chemotaxis in a NOX2-dependent manner. Migration using the EZ-TAXIScan device was determined in WT, TREM-1-deficient, CYBB-deficient, and TREM-1/CYBB-deficient neutrophils stimulated with fMLP or ZAS in the presence or absence of 10 μ M DPI. Motility (A), CI (B and C), and instantaneous velocity (D) were measured. Data from 4–12 independent experiments were compiled and shown as Mean ± SEM; each data point represents 3–5 pooled mice. * P

    Journal: Journal of leukocyte biology

    Article Title: TREM-1 regulates neutrophil chemotaxis by promoting NOX-dependent superoxide production

    doi: 10.1002/JLB.3VMA0918-375R

    Figure Lengend Snippet: TREM-1 deficiency impairs neutrophil chemotaxis in a NOX2-dependent manner. Migration using the EZ-TAXIScan device was determined in WT, TREM-1-deficient, CYBB-deficient, and TREM-1/CYBB-deficient neutrophils stimulated with fMLP or ZAS in the presence or absence of 10 μ M DPI. Motility (A), CI (B and C), and instantaneous velocity (D) were measured. Data from 4–12 independent experiments were compiled and shown as Mean ± SEM; each data point represents 3–5 pooled mice. * P

    Article Snippet: Genotypes were determined by PCR for both Trem1/3 and Cybb and confirmed by FACs analysis of blood for TREM-1, using anti-mouse TREM-1, clone 174031 (R & D Systems), and dihydrorhodamine (DHR; Thermofisher Scientific) for ROS production with PMA (Sigma) stimulation.

    Techniques: Chemotaxis Assay, Migration, Mouse Assay

    TREM-1 deficiency attenuates superoxide production in response to fMLP. Superoxide generated by WT ( A ) and TREM-1-deficient (B) neutrophils stimulated with fMLP (100 μ ” section. (C) Peak superoxide generation for each treatment. Mean ± SEM of relative light units of 6 replicates of 3–5 pooled mice. * P

    Journal: Journal of leukocyte biology

    Article Title: TREM-1 regulates neutrophil chemotaxis by promoting NOX-dependent superoxide production

    doi: 10.1002/JLB.3VMA0918-375R

    Figure Lengend Snippet: TREM-1 deficiency attenuates superoxide production in response to fMLP. Superoxide generated by WT ( A ) and TREM-1-deficient (B) neutrophils stimulated with fMLP (100 μ ” section. (C) Peak superoxide generation for each treatment. Mean ± SEM of relative light units of 6 replicates of 3–5 pooled mice. * P

    Article Snippet: Genotypes were determined by PCR for both Trem1/3 and Cybb and confirmed by FACs analysis of blood for TREM-1, using anti-mouse TREM-1, clone 174031 (R & D Systems), and dihydrorhodamine (DHR; Thermofisher Scientific) for ROS production with PMA (Sigma) stimulation.

    Techniques: Generated, Mouse Assay

    TREM-1 deficiency attenuates AKT activation. WT and TREM-1-deficient neutrophils were stimulated for the indicated times with OpZ and the phosphorylation of AKT, ERK1/2, and p38MAPK was determined. (A) Immunoblots from 1 representative experiment out of 3 are shown. (B) Quantitation of phosphorylated and total kinase levels of all 3 time course experiments. (C) WT and TREM-1-deficient neutrophils were stimulated for 15 min with OpZ and AKT activation determined. Quantitation of phosphorylated and total AKT levels is shown as fold increase relative to resting levels. Each data point represents Mean ± SEM of 3–5 pooled mice, N = 5 independent experiments; * P

    Journal: Journal of leukocyte biology

    Article Title: TREM-1 regulates neutrophil chemotaxis by promoting NOX-dependent superoxide production

    doi: 10.1002/JLB.3VMA0918-375R

    Figure Lengend Snippet: TREM-1 deficiency attenuates AKT activation. WT and TREM-1-deficient neutrophils were stimulated for the indicated times with OpZ and the phosphorylation of AKT, ERK1/2, and p38MAPK was determined. (A) Immunoblots from 1 representative experiment out of 3 are shown. (B) Quantitation of phosphorylated and total kinase levels of all 3 time course experiments. (C) WT and TREM-1-deficient neutrophils were stimulated for 15 min with OpZ and AKT activation determined. Quantitation of phosphorylated and total AKT levels is shown as fold increase relative to resting levels. Each data point represents Mean ± SEM of 3–5 pooled mice, N = 5 independent experiments; * P

    Article Snippet: Genotypes were determined by PCR for both Trem1/3 and Cybb and confirmed by FACs analysis of blood for TREM-1, using anti-mouse TREM-1, clone 174031 (R & D Systems), and dihydrorhodamine (DHR; Thermofisher Scientific) for ROS production with PMA (Sigma) stimulation.

    Techniques: Activation Assay, Western Blot, Quantitation Assay, Mouse Assay

    TREM-1 deficiency attenuates oxygen consumption independently of mitochondrial respiration. (A) Oxygen consumption in WT and TREM-1-deficient neutrophils was determined using the Clark electrode. Data from 4 representative experiments are shown as Mean ± SEM of 3–5 pooled mice/data point. * P

    Journal: Journal of leukocyte biology

    Article Title: TREM-1 regulates neutrophil chemotaxis by promoting NOX-dependent superoxide production

    doi: 10.1002/JLB.3VMA0918-375R

    Figure Lengend Snippet: TREM-1 deficiency attenuates oxygen consumption independently of mitochondrial respiration. (A) Oxygen consumption in WT and TREM-1-deficient neutrophils was determined using the Clark electrode. Data from 4 representative experiments are shown as Mean ± SEM of 3–5 pooled mice/data point. * P

    Article Snippet: Genotypes were determined by PCR for both Trem1/3 and Cybb and confirmed by FACs analysis of blood for TREM-1, using anti-mouse TREM-1, clone 174031 (R & D Systems), and dihydrorhodamine (DHR; Thermofisher Scientific) for ROS production with PMA (Sigma) stimulation.

    Techniques: Mouse Assay

    a – d TNF-α, IFN-γ, IL-10 and IL-6 concentrations of control and treated malarial mice and effect of mTREM-1/Ab and rmTREM-1/Fc on the production of TNF-α, IFN-γ, IL-10 and IL-6 in malaria-infected mice. Each column represents the mean ± SEM of 8 mice. C + NS = control + normal saline; M + NS = malaria + normal saline; M + mTREM-1/Ab = malaria + mouse TREM-1 antibody; M + rmTREM-1/Fc = malaria + recombinant TREM-1 Fc. * P

    Journal: Journal of Parasitic Diseases: Official Organ of the Indian Society for Parasitology

    Article Title: TREM-1 modulation produces positive outcome on the histopathology and cytokines release profile of Plasmodium berghei-infected mice

    doi: 10.1007/s12639-018-1070-3

    Figure Lengend Snippet: a – d TNF-α, IFN-γ, IL-10 and IL-6 concentrations of control and treated malarial mice and effect of mTREM-1/Ab and rmTREM-1/Fc on the production of TNF-α, IFN-γ, IL-10 and IL-6 in malaria-infected mice. Each column represents the mean ± SEM of 8 mice. C + NS = control + normal saline; M + NS = malaria + normal saline; M + mTREM-1/Ab = malaria + mouse TREM-1 antibody; M + rmTREM-1/Fc = malaria + recombinant TREM-1 Fc. * P

    Article Snippet: Meanwhile, recombinant mouse TREM-1 Fc Chimera (rmTREM-1/Fc) (R & D Systems Inc. Minneapollis, US) used in this study was a mouse recombinant fusion protein that protects the mice against LPS-induced shock. rmTREM-1/Fc was supplied in lyophilized form in 108 µL of a filtered solution in phosphate-buffer saline (PBS) with pH 7.4.

    Techniques: Mouse Assay, Infection, Recombinant

    TREM-1 concentrations in the plasma of control and malarial mice. The infected mice were inoculated with 2 × 10 7 PRBC (i.v.) from a donor mouse previously infected with P. berghei ANKA. Control mice received an equivalent volume and dilution (0.2 mL/animal) of normal mouse red blood cells. TREM-1 concentrations were determined in the plasma of control and malaria-infected mice. Results were expressed as the mean ± SEM (N = 8). * P

    Journal: Journal of Parasitic Diseases: Official Organ of the Indian Society for Parasitology

    Article Title: TREM-1 modulation produces positive outcome on the histopathology and cytokines release profile of Plasmodium berghei-infected mice

    doi: 10.1007/s12639-018-1070-3

    Figure Lengend Snippet: TREM-1 concentrations in the plasma of control and malarial mice. The infected mice were inoculated with 2 × 10 7 PRBC (i.v.) from a donor mouse previously infected with P. berghei ANKA. Control mice received an equivalent volume and dilution (0.2 mL/animal) of normal mouse red blood cells. TREM-1 concentrations were determined in the plasma of control and malaria-infected mice. Results were expressed as the mean ± SEM (N = 8). * P

    Article Snippet: Meanwhile, recombinant mouse TREM-1 Fc Chimera (rmTREM-1/Fc) (R & D Systems Inc. Minneapollis, US) used in this study was a mouse recombinant fusion protein that protects the mice against LPS-induced shock. rmTREM-1/Fc was supplied in lyophilized form in 108 µL of a filtered solution in phosphate-buffer saline (PBS) with pH 7.4.

    Techniques: Mouse Assay, Infection

    Correlation between the increase in percentage parasitemia and plasma TREM-1 concentration (pg/mL) in malaria-infected mice. The infected animals were inoculated with 2 × 10 7 PRBC (i.v.) from a donor mouse previously infected with P. berghei ANKA. The correlation coefficient was analyzed by using linear regression of Pearson’s rank order correlation coefficient

    Journal: Journal of Parasitic Diseases: Official Organ of the Indian Society for Parasitology

    Article Title: TREM-1 modulation produces positive outcome on the histopathology and cytokines release profile of Plasmodium berghei-infected mice

    doi: 10.1007/s12639-018-1070-3

    Figure Lengend Snippet: Correlation between the increase in percentage parasitemia and plasma TREM-1 concentration (pg/mL) in malaria-infected mice. The infected animals were inoculated with 2 × 10 7 PRBC (i.v.) from a donor mouse previously infected with P. berghei ANKA. The correlation coefficient was analyzed by using linear regression of Pearson’s rank order correlation coefficient

    Article Snippet: Meanwhile, recombinant mouse TREM-1 Fc Chimera (rmTREM-1/Fc) (R & D Systems Inc. Minneapollis, US) used in this study was a mouse recombinant fusion protein that protects the mice against LPS-induced shock. rmTREM-1/Fc was supplied in lyophilized form in 108 µL of a filtered solution in phosphate-buffer saline (PBS) with pH 7.4.

    Techniques: Concentration Assay, Infection, Mouse Assay

    Effects of modulating TREM-1 release on survival rate of treated malaria-infected mice with mTREM-1/Ab and mTREM-1/Fc (n = 8) in three separate experiments. Data were analysed by Kaplan–Meier survival estimator. Keynote: C = control, NS = normal saline, M = malaria, mTREM-1/Ab = mouse TREM-1 polyclonal antibody, mTREM-1/Fc = recombinant mouse TREM-1 Fc chimera

    Journal: Journal of Parasitic Diseases: Official Organ of the Indian Society for Parasitology

    Article Title: TREM-1 modulation produces positive outcome on the histopathology and cytokines release profile of Plasmodium berghei-infected mice

    doi: 10.1007/s12639-018-1070-3

    Figure Lengend Snippet: Effects of modulating TREM-1 release on survival rate of treated malaria-infected mice with mTREM-1/Ab and mTREM-1/Fc (n = 8) in three separate experiments. Data were analysed by Kaplan–Meier survival estimator. Keynote: C = control, NS = normal saline, M = malaria, mTREM-1/Ab = mouse TREM-1 polyclonal antibody, mTREM-1/Fc = recombinant mouse TREM-1 Fc chimera

    Article Snippet: Meanwhile, recombinant mouse TREM-1 Fc Chimera (rmTREM-1/Fc) (R & D Systems Inc. Minneapollis, US) used in this study was a mouse recombinant fusion protein that protects the mice against LPS-induced shock. rmTREM-1/Fc was supplied in lyophilized form in 108 µL of a filtered solution in phosphate-buffer saline (PBS) with pH 7.4.

    Techniques: Infection, Mouse Assay, Recombinant

    Percentage parasitemia of control, malarial with saline, and malaria-infected mice with TREM-1 antibody treatments. The infected animals were inoculated with 2 × 10 7 PRBC (i.v) from a donor mouse previously infected with P. berghei ANKA. The treatment animals were injected with TREM-1 antibody, 10 µg per animal in 0.2 mL volume. Control animals received an equivalent volume and dilution (0.2 mL/animal) of normal mouse red blood cells. Results were expressed as the mean ± SEM (N = 8). * P

    Journal: Journal of Parasitic Diseases: Official Organ of the Indian Society for Parasitology

    Article Title: TREM-1 modulation produces positive outcome on the histopathology and cytokines release profile of Plasmodium berghei-infected mice

    doi: 10.1007/s12639-018-1070-3

    Figure Lengend Snippet: Percentage parasitemia of control, malarial with saline, and malaria-infected mice with TREM-1 antibody treatments. The infected animals were inoculated with 2 × 10 7 PRBC (i.v) from a donor mouse previously infected with P. berghei ANKA. The treatment animals were injected with TREM-1 antibody, 10 µg per animal in 0.2 mL volume. Control animals received an equivalent volume and dilution (0.2 mL/animal) of normal mouse red blood cells. Results were expressed as the mean ± SEM (N = 8). * P

    Article Snippet: Meanwhile, recombinant mouse TREM-1 Fc Chimera (rmTREM-1/Fc) (R & D Systems Inc. Minneapollis, US) used in this study was a mouse recombinant fusion protein that protects the mice against LPS-induced shock. rmTREM-1/Fc was supplied in lyophilized form in 108 µL of a filtered solution in phosphate-buffer saline (PBS) with pH 7.4.

    Techniques: Infection, Mouse Assay, Injection

    Summary of findings. Sepsis causes an increased release of eCIRP. The endogenous ligand eCIRP recognizes TREM-1 and activates intracellular signaling molecules DAP12 and Syk, leading to increased expression of proinflammatory mediators that cause excessive inflammation and remote tissue injury. eCIRP increases TREM-1 expression, possibly via positive feedback induction. A small peptide, M3, derived from human eCIRP abrogates eCIRP–TREM-1 interaction, thereby leading to decreased inflammation and attenuated ALI.

    Journal: JCI Insight

    Article Title: Extracellular CIRP as an endogenous TREM-1 ligand to fuel inflammation in sepsis

    doi: 10.1172/jci.insight.134172

    Figure Lengend Snippet: Summary of findings. Sepsis causes an increased release of eCIRP. The endogenous ligand eCIRP recognizes TREM-1 and activates intracellular signaling molecules DAP12 and Syk, leading to increased expression of proinflammatory mediators that cause excessive inflammation and remote tissue injury. eCIRP increases TREM-1 expression, possibly via positive feedback induction. A small peptide, M3, derived from human eCIRP abrogates eCIRP–TREM-1 interaction, thereby leading to decreased inflammation and attenuated ALI.

    Article Snippet: TREM-1 (recombinant mouse TREM-1–Fc Chimera, R & D Systems, Bio-Techne, catalog 1187-TR-025) was injected as an analyte in concentrations of 0 to 500 nM.

    Techniques: Expressing, Derivative Assay

    TREM-1 deficiency ameliorates eCIRP-mediated inflammation. Primary peritoneal macrophages were isolated from WT and TREM-1 –/– mice and were stimulated with PBS or rmCIRP (1 μg/mL). After 24 hours, ( A ) TNF-α and ( B ) IL-6 in culture supernatants were measured by ELISA. Data are expressed as mean ± SEM; n = 12 wells/group. Multiple groups were compared by 1-way ANOVA and Tukey’s method (* P

    Journal: JCI Insight

    Article Title: Extracellular CIRP as an endogenous TREM-1 ligand to fuel inflammation in sepsis

    doi: 10.1172/jci.insight.134172

    Figure Lengend Snippet: TREM-1 deficiency ameliorates eCIRP-mediated inflammation. Primary peritoneal macrophages were isolated from WT and TREM-1 –/– mice and were stimulated with PBS or rmCIRP (1 μg/mL). After 24 hours, ( A ) TNF-α and ( B ) IL-6 in culture supernatants were measured by ELISA. Data are expressed as mean ± SEM; n = 12 wells/group. Multiple groups were compared by 1-way ANOVA and Tukey’s method (* P

    Article Snippet: TREM-1 (recombinant mouse TREM-1–Fc Chimera, R & D Systems, Bio-Techne, catalog 1187-TR-025) was injected as an analyte in concentrations of 0 to 500 nM.

    Techniques: Isolation, Mouse Assay, Enzyme-linked Immunosorbent Assay

    eCIRP binds TREM-1 to promote inflammation. ( A ) SPR between rmCIRP and rmTREM-1. Anti-his antibody was used to capture rmCIRP-his. rmTREM-1 was injected as an analyte in concentrations of 0 to 500 nM. ( B ) RAW264.7 cells were treated with rmCIRP (5 μg/mL) at 4°C for 10 minutes, fixed in a nonpermeabilized fashion, and stained with primary antibodies against CIRP, TREM-1, and CD-11b as well as fluorescently labeled secondary antibodies. Confocal microscopy images were obtained with a 63× objective. Colocalization is indicated by the yellow color. ( C ) After the staining protocol described in B , cell-associated fluorescence was measured. The transfer of fluorescence was calculated as FRET units. Data are expressed as mean ± SEM obtained from 3 independent experiments; n = 8–9/group. Groups compared by unpaired t test (* P

    Journal: JCI Insight

    Article Title: Extracellular CIRP as an endogenous TREM-1 ligand to fuel inflammation in sepsis

    doi: 10.1172/jci.insight.134172

    Figure Lengend Snippet: eCIRP binds TREM-1 to promote inflammation. ( A ) SPR between rmCIRP and rmTREM-1. Anti-his antibody was used to capture rmCIRP-his. rmTREM-1 was injected as an analyte in concentrations of 0 to 500 nM. ( B ) RAW264.7 cells were treated with rmCIRP (5 μg/mL) at 4°C for 10 minutes, fixed in a nonpermeabilized fashion, and stained with primary antibodies against CIRP, TREM-1, and CD-11b as well as fluorescently labeled secondary antibodies. Confocal microscopy images were obtained with a 63× objective. Colocalization is indicated by the yellow color. ( C ) After the staining protocol described in B , cell-associated fluorescence was measured. The transfer of fluorescence was calculated as FRET units. Data are expressed as mean ± SEM obtained from 3 independent experiments; n = 8–9/group. Groups compared by unpaired t test (* P

    Article Snippet: TREM-1 (recombinant mouse TREM-1–Fc Chimera, R & D Systems, Bio-Techne, catalog 1187-TR-025) was injected as an analyte in concentrations of 0 to 500 nM.

    Techniques: SPR Assay, Injection, Staining, Labeling, Confocal Microscopy, Fluorescence