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mouse cytokine array panel a  (R&D Systems)


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    Structured Review

    R&D Systems mouse cytokine array panel a
    <t>Cytokine</t> profiling showed significantly elevated levels of (A) CXCL10/IP-10 (1.37-fold increase; p < 0.0001, n = 3) and TIMP-1 (1.35-fold increase; p < 0.0001, n = 3) in the CD38-OE group compared to the CD38-WT group, and (B) ICAM-1, with a 1.15-fold increase compared to the CD38-WT group and a 1.34-fold increase compared to the control group (p < 0.0002, n = 3). No significant changes were observed in SDF-1/CXCL12 expression. (n = 3). These molecules were highlighted for their notable, yet relatively understudied, roles in GBM progression and tumor microenvironment modulation compared to other cytokines in the panel, which have more established functions in cancer biology. One-way ANOVA with Tukey’s post-hoc, *p < 0.0001, **p < 0.0002.
    Mouse Cytokine Array Panel A, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 651 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+proteome+profiler+array/pmc13090310-102-4-11?v=R%26D+Systems
    Average 96 stars, based on 651 article reviews
    mouse cytokine array panel a - by Bioz Stars, 2026-07
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    Images

    1) Product Images from "CD38 overexpression drives glioblastoma progression via L1CAM/ICAM1/JAK-STAT-Driven tumor microenvironment rewiring"

    Article Title: CD38 overexpression drives glioblastoma progression via L1CAM/ICAM1/JAK-STAT-Driven tumor microenvironment rewiring

    Journal: Translational Oncology

    doi: 10.1016/j.tranon.2026.102758

    Cytokine profiling showed significantly elevated levels of (A) CXCL10/IP-10 (1.37-fold increase; p < 0.0001, n = 3) and TIMP-1 (1.35-fold increase; p < 0.0001, n = 3) in the CD38-OE group compared to the CD38-WT group, and (B) ICAM-1, with a 1.15-fold increase compared to the CD38-WT group and a 1.34-fold increase compared to the control group (p < 0.0002, n = 3). No significant changes were observed in SDF-1/CXCL12 expression. (n = 3). These molecules were highlighted for their notable, yet relatively understudied, roles in GBM progression and tumor microenvironment modulation compared to other cytokines in the panel, which have more established functions in cancer biology. One-way ANOVA with Tukey’s post-hoc, *p < 0.0001, **p < 0.0002.
    Figure Legend Snippet: Cytokine profiling showed significantly elevated levels of (A) CXCL10/IP-10 (1.37-fold increase; p < 0.0001, n = 3) and TIMP-1 (1.35-fold increase; p < 0.0001, n = 3) in the CD38-OE group compared to the CD38-WT group, and (B) ICAM-1, with a 1.15-fold increase compared to the CD38-WT group and a 1.34-fold increase compared to the control group (p < 0.0002, n = 3). No significant changes were observed in SDF-1/CXCL12 expression. (n = 3). These molecules were highlighted for their notable, yet relatively understudied, roles in GBM progression and tumor microenvironment modulation compared to other cytokines in the panel, which have more established functions in cancer biology. One-way ANOVA with Tukey’s post-hoc, *p < 0.0001, **p < 0.0002.

    Techniques Used: Control, Expressing



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    R&D Systems proteome profiler mouse xl cytokine array kit
    (A) Representative Western blots clearly show the upregulation of PAD4 and H3Cit in 4-week-old Dsg2 mut/mut cardiac lysates. (B) Quantification of western blots from . Data presented as mean±SEM; n=4 mice/parameter; ***P<0.001 and ****P<0.0001 via two-tailed T-test. (C) Representative ECG tracings from WT, Dsg2 mut/mut , and Dsg2 mut/mut ; Pad4 -/- at 16-weeks of age, respectively. (D) Percent ectopic beats at 16-weeks of age. Data presented as mean±SEM; n≥7. Statistical significance was determined via one-way ANOVA with Tukey’s multiple comparison test (**P<0.01 and ***P<0.001). (E) Percent left ventricular ejection fraction at 16-weeks of age. (F) Percent left ventricular fractional shortening at 16-weeks of age. (G) Stroke Volume at 16-weeks of age. (H) Representative Masson’s trichrome-immunostained hearts from Dsg2 mut/mut and Dsg2 mut/mut ; Pad4 -/- at 16-weeks of age. (I) Percent fibrosis at 16-weeks of age. Data presented as mean±SEM; n≥12. Statistical significance was determined via one-way ANOVA with Tukey’s multiple comparison test for E-G and via two-tailed T-test for I (*P<0.05, ***P<0.001, and ****P<0.0001). (J) Representative <t>cytokine</t> arrays with legend for key cytokines from WT, Dsg2 mut/mut , and Dsg2 mut/mut ; Pad4 -/- mice. (K) Legend of selected cytokines. (L-N) Quantification of selected cytokines normalized to reference band in WT, Dsg2 mut/mut , and Dsg2 mut/mut ; Pad4 -/- mice. Data presented as mean±SEM; n=4. *P<0.05, via two-tailed T-test. C5/C5a, Complement Component C5/C5a; MCP-1, Monocyte Chemoattractant Protein-1; MIP-α/β, Macrophage Inflammatory Protein-1 alpha/beta; MMP-3, Matrix metalloproteinase-3; MMP-9, Matrix metalloproteinase-9; MPO, Myeloperoxidase; NGAL, Neutrophil gelatinase-associated lipocalin; TNFα, Tumor Necrosis Factor-alpha; and OPN, Osteopontin.
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    (A) Representative Western blots clearly show the upregulation of PAD4 and H3Cit in 4-week-old Dsg2 mut/mut cardiac lysates. (B) Quantification of western blots from . Data presented as mean±SEM; n=4 mice/parameter; ***P<0.001 and ****P<0.0001 via two-tailed T-test. (C) Representative ECG tracings from WT, Dsg2 mut/mut , and Dsg2 mut/mut ; Pad4 -/- at 16-weeks of age, respectively. (D) Percent ectopic beats at 16-weeks of age. Data presented as mean±SEM; n≥7. Statistical significance was determined via one-way ANOVA with Tukey’s multiple comparison test (**P<0.01 and ***P<0.001). (E) Percent left ventricular ejection fraction at 16-weeks of age. (F) Percent left ventricular fractional shortening at 16-weeks of age. (G) Stroke Volume at 16-weeks of age. (H) Representative Masson’s trichrome-immunostained hearts from Dsg2 mut/mut and Dsg2 mut/mut ; Pad4 -/- at 16-weeks of age. (I) Percent fibrosis at 16-weeks of age. Data presented as mean±SEM; n≥12. Statistical significance was determined via one-way ANOVA with Tukey’s multiple comparison test for E-G and via two-tailed T-test for I (*P<0.05, ***P<0.001, and ****P<0.0001). (J) Representative <t>cytokine</t> arrays with legend for key cytokines from WT, Dsg2 mut/mut , and Dsg2 mut/mut ; Pad4 -/- mice. (K) Legend of selected cytokines. (L-N) Quantification of selected cytokines normalized to reference band in WT, Dsg2 mut/mut , and Dsg2 mut/mut ; Pad4 -/- mice. Data presented as mean±SEM; n=4. *P<0.05, via two-tailed T-test. C5/C5a, Complement Component C5/C5a; MCP-1, Monocyte Chemoattractant Protein-1; MIP-α/β, Macrophage Inflammatory Protein-1 alpha/beta; MMP-3, Matrix metalloproteinase-3; MMP-9, Matrix metalloproteinase-9; MPO, Myeloperoxidase; NGAL, Neutrophil gelatinase-associated lipocalin; TNFα, Tumor Necrosis Factor-alpha; and OPN, Osteopontin.
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    R&D Systems proteome profiler mouse xl cytokine array
    (A) Representative Western blots clearly show the upregulation of PAD4 and H3Cit in 4-week-old Dsg2 mut/mut cardiac lysates. (B) Quantification of western blots from . Data presented as mean±SEM; n=4 mice/parameter; ***P<0.001 and ****P<0.0001 via two-tailed T-test. (C) Representative ECG tracings from WT, Dsg2 mut/mut , and Dsg2 mut/mut ; Pad4 -/- at 16-weeks of age, respectively. (D) Percent ectopic beats at 16-weeks of age. Data presented as mean±SEM; n≥7. Statistical significance was determined via one-way ANOVA with Tukey’s multiple comparison test (**P<0.01 and ***P<0.001). (E) Percent left ventricular ejection fraction at 16-weeks of age. (F) Percent left ventricular fractional shortening at 16-weeks of age. (G) Stroke Volume at 16-weeks of age. (H) Representative Masson’s trichrome-immunostained hearts from Dsg2 mut/mut and Dsg2 mut/mut ; Pad4 -/- at 16-weeks of age. (I) Percent fibrosis at 16-weeks of age. Data presented as mean±SEM; n≥12. Statistical significance was determined via one-way ANOVA with Tukey’s multiple comparison test for E-G and via two-tailed T-test for I (*P<0.05, ***P<0.001, and ****P<0.0001). (J) Representative <t>cytokine</t> arrays with legend for key cytokines from WT, Dsg2 mut/mut , and Dsg2 mut/mut ; Pad4 -/- mice. (K) Legend of selected cytokines. (L-N) Quantification of selected cytokines normalized to reference band in WT, Dsg2 mut/mut , and Dsg2 mut/mut ; Pad4 -/- mice. Data presented as mean±SEM; n=4. *P<0.05, via two-tailed T-test. C5/C5a, Complement Component C5/C5a; MCP-1, Monocyte Chemoattractant Protein-1; MIP-α/β, Macrophage Inflammatory Protein-1 alpha/beta; MMP-3, Matrix metalloproteinase-3; MMP-9, Matrix metalloproteinase-9; MPO, Myeloperoxidase; NGAL, Neutrophil gelatinase-associated lipocalin; TNFα, Tumor Necrosis Factor-alpha; and OPN, Osteopontin.
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    Image Search Results


    Cytokine profiling showed significantly elevated levels of (A) CXCL10/IP-10 (1.37-fold increase; p < 0.0001, n = 3) and TIMP-1 (1.35-fold increase; p < 0.0001, n = 3) in the CD38-OE group compared to the CD38-WT group, and (B) ICAM-1, with a 1.15-fold increase compared to the CD38-WT group and a 1.34-fold increase compared to the control group (p < 0.0002, n = 3). No significant changes were observed in SDF-1/CXCL12 expression. (n = 3). These molecules were highlighted for their notable, yet relatively understudied, roles in GBM progression and tumor microenvironment modulation compared to other cytokines in the panel, which have more established functions in cancer biology. One-way ANOVA with Tukey’s post-hoc, *p < 0.0001, **p < 0.0002.

    Journal: Translational Oncology

    Article Title: CD38 overexpression drives glioblastoma progression via L1CAM/ICAM1/JAK-STAT-Driven tumor microenvironment rewiring

    doi: 10.1016/j.tranon.2026.102758

    Figure Lengend Snippet: Cytokine profiling showed significantly elevated levels of (A) CXCL10/IP-10 (1.37-fold increase; p < 0.0001, n = 3) and TIMP-1 (1.35-fold increase; p < 0.0001, n = 3) in the CD38-OE group compared to the CD38-WT group, and (B) ICAM-1, with a 1.15-fold increase compared to the CD38-WT group and a 1.34-fold increase compared to the control group (p < 0.0002, n = 3). No significant changes were observed in SDF-1/CXCL12 expression. (n = 3). These molecules were highlighted for their notable, yet relatively understudied, roles in GBM progression and tumor microenvironment modulation compared to other cytokines in the panel, which have more established functions in cancer biology. One-way ANOVA with Tukey’s post-hoc, *p < 0.0001, **p < 0.0002.

    Article Snippet: For cytokine profiling, the Mouse Cytokine Array Panel A (Catalog #ARY006, R&D Systems, USA) was used according to the manufacturer’s instructions (Supplementary Table).

    Techniques: Control, Expressing

    (A) Representative Western blots clearly show the upregulation of PAD4 and H3Cit in 4-week-old Dsg2 mut/mut cardiac lysates. (B) Quantification of western blots from . Data presented as mean±SEM; n=4 mice/parameter; ***P<0.001 and ****P<0.0001 via two-tailed T-test. (C) Representative ECG tracings from WT, Dsg2 mut/mut , and Dsg2 mut/mut ; Pad4 -/- at 16-weeks of age, respectively. (D) Percent ectopic beats at 16-weeks of age. Data presented as mean±SEM; n≥7. Statistical significance was determined via one-way ANOVA with Tukey’s multiple comparison test (**P<0.01 and ***P<0.001). (E) Percent left ventricular ejection fraction at 16-weeks of age. (F) Percent left ventricular fractional shortening at 16-weeks of age. (G) Stroke Volume at 16-weeks of age. (H) Representative Masson’s trichrome-immunostained hearts from Dsg2 mut/mut and Dsg2 mut/mut ; Pad4 -/- at 16-weeks of age. (I) Percent fibrosis at 16-weeks of age. Data presented as mean±SEM; n≥12. Statistical significance was determined via one-way ANOVA with Tukey’s multiple comparison test for E-G and via two-tailed T-test for I (*P<0.05, ***P<0.001, and ****P<0.0001). (J) Representative cytokine arrays with legend for key cytokines from WT, Dsg2 mut/mut , and Dsg2 mut/mut ; Pad4 -/- mice. (K) Legend of selected cytokines. (L-N) Quantification of selected cytokines normalized to reference band in WT, Dsg2 mut/mut , and Dsg2 mut/mut ; Pad4 -/- mice. Data presented as mean±SEM; n=4. *P<0.05, via two-tailed T-test. C5/C5a, Complement Component C5/C5a; MCP-1, Monocyte Chemoattractant Protein-1; MIP-α/β, Macrophage Inflammatory Protein-1 alpha/beta; MMP-3, Matrix metalloproteinase-3; MMP-9, Matrix metalloproteinase-9; MPO, Myeloperoxidase; NGAL, Neutrophil gelatinase-associated lipocalin; TNFα, Tumor Necrosis Factor-alpha; and OPN, Osteopontin.

    Journal: bioRxiv

    Article Title: NETosis and Myeloperoxidase Promotes Inflammation and Cardiac Remodeling in Arrhythmogenic Cardiomyopathy

    doi: 10.64898/2026.04.14.718596

    Figure Lengend Snippet: (A) Representative Western blots clearly show the upregulation of PAD4 and H3Cit in 4-week-old Dsg2 mut/mut cardiac lysates. (B) Quantification of western blots from . Data presented as mean±SEM; n=4 mice/parameter; ***P<0.001 and ****P<0.0001 via two-tailed T-test. (C) Representative ECG tracings from WT, Dsg2 mut/mut , and Dsg2 mut/mut ; Pad4 -/- at 16-weeks of age, respectively. (D) Percent ectopic beats at 16-weeks of age. Data presented as mean±SEM; n≥7. Statistical significance was determined via one-way ANOVA with Tukey’s multiple comparison test (**P<0.01 and ***P<0.001). (E) Percent left ventricular ejection fraction at 16-weeks of age. (F) Percent left ventricular fractional shortening at 16-weeks of age. (G) Stroke Volume at 16-weeks of age. (H) Representative Masson’s trichrome-immunostained hearts from Dsg2 mut/mut and Dsg2 mut/mut ; Pad4 -/- at 16-weeks of age. (I) Percent fibrosis at 16-weeks of age. Data presented as mean±SEM; n≥12. Statistical significance was determined via one-way ANOVA with Tukey’s multiple comparison test for E-G and via two-tailed T-test for I (*P<0.05, ***P<0.001, and ****P<0.0001). (J) Representative cytokine arrays with legend for key cytokines from WT, Dsg2 mut/mut , and Dsg2 mut/mut ; Pad4 -/- mice. (K) Legend of selected cytokines. (L-N) Quantification of selected cytokines normalized to reference band in WT, Dsg2 mut/mut , and Dsg2 mut/mut ; Pad4 -/- mice. Data presented as mean±SEM; n=4. *P<0.05, via two-tailed T-test. C5/C5a, Complement Component C5/C5a; MCP-1, Monocyte Chemoattractant Protein-1; MIP-α/β, Macrophage Inflammatory Protein-1 alpha/beta; MMP-3, Matrix metalloproteinase-3; MMP-9, Matrix metalloproteinase-9; MPO, Myeloperoxidase; NGAL, Neutrophil gelatinase-associated lipocalin; TNFα, Tumor Necrosis Factor-alpha; and OPN, Osteopontin.

    Article Snippet: Cardiac cytokine profiling was conducted using the Proteome Profiler Mouse XL Cytokine Array Kit (R&D Systems, Cat. No. ARY028) as previously described.

    Techniques: Western Blot, Two Tailed Test, Comparison

    (A) Schematic timeline of PF1355 treatment and in vivo mouse measurements. (B) Percent left ventricular ejection fraction (%LVEF) at 16-weeks of age. (C) Percent left ventricular fractional shortening (%FS) at 16-weeks of age. Data presented as mean±SEM; n≥5. Statistical significance was determined via two-way ANOVA with Tukey’s multiple comparison test (*P<0.05 and **P<0.01). (D) Representative ECG tracings from PF1355 treated Dsg2 mut/mut , Placebo treated Dsg2 mut/mut , and WT at 16-weeks of age, respectively. Asterisks, ectopic beats. (E) Percent ectopic beats (% Ectopics), (F) R-amplitude, and (G) Q-amplitude at 16-weeks of age. (H) Representative Masson’s trichrome-immunostained hearts from Placebo-treated and PF1355-treated Dsg2 mut/mut at 16-weeks of age. (I) Percent fibrosis at 16-weeks of age. Data presented as mean±SEM; n≥6. Statistical significance was determined via Welch’s t-test for E and one-way ANOVA with Tukey’s multiple comparison test for F,G, and I (*P<0.05). (J) Representative cytokine arrays with legend for key cytokines from Placebo-treated and PF1355-treated Dsg2 mut/mut , and WT mice. (K) Legend of selected cytokines. (L-N) Quantification of selected cytokines normalized to reference band in PF1355-treated and Placebo-treated Dsg2 mut/mut , and WT mice. Data presented as mean±SEM; n=4. *P<0.05, via two-tailed T-test. C5/C5a, Complement Component C5/C5a; CCL11, C-C motif chemokine ligand 11; CCL12, C-C motif chemokine ligand 12; LIX, Lipopolysaccharide-induced CXC chemokine; MCP-1, Monocyte Chemoattractant Protein-1; MIP-α/β, Macrophage Inflammatory Protein-1 alpha/beta; MMP-3, Matrix metalloproteinase-3; MMP-9, Matrix metalloproteinase-9; and NGAL, Neutrophil gelatinase-associated lipocalin. All data presented as mean±SEM. Statistical significance was determined via two-way ANOVA with Tukey’s multiple comparison test for B-C and via two-tailed T-test for E-G, I, and L-N (*P<0.05).

    Journal: bioRxiv

    Article Title: NETosis and Myeloperoxidase Promotes Inflammation and Cardiac Remodeling in Arrhythmogenic Cardiomyopathy

    doi: 10.64898/2026.04.14.718596

    Figure Lengend Snippet: (A) Schematic timeline of PF1355 treatment and in vivo mouse measurements. (B) Percent left ventricular ejection fraction (%LVEF) at 16-weeks of age. (C) Percent left ventricular fractional shortening (%FS) at 16-weeks of age. Data presented as mean±SEM; n≥5. Statistical significance was determined via two-way ANOVA with Tukey’s multiple comparison test (*P<0.05 and **P<0.01). (D) Representative ECG tracings from PF1355 treated Dsg2 mut/mut , Placebo treated Dsg2 mut/mut , and WT at 16-weeks of age, respectively. Asterisks, ectopic beats. (E) Percent ectopic beats (% Ectopics), (F) R-amplitude, and (G) Q-amplitude at 16-weeks of age. (H) Representative Masson’s trichrome-immunostained hearts from Placebo-treated and PF1355-treated Dsg2 mut/mut at 16-weeks of age. (I) Percent fibrosis at 16-weeks of age. Data presented as mean±SEM; n≥6. Statistical significance was determined via Welch’s t-test for E and one-way ANOVA with Tukey’s multiple comparison test for F,G, and I (*P<0.05). (J) Representative cytokine arrays with legend for key cytokines from Placebo-treated and PF1355-treated Dsg2 mut/mut , and WT mice. (K) Legend of selected cytokines. (L-N) Quantification of selected cytokines normalized to reference band in PF1355-treated and Placebo-treated Dsg2 mut/mut , and WT mice. Data presented as mean±SEM; n=4. *P<0.05, via two-tailed T-test. C5/C5a, Complement Component C5/C5a; CCL11, C-C motif chemokine ligand 11; CCL12, C-C motif chemokine ligand 12; LIX, Lipopolysaccharide-induced CXC chemokine; MCP-1, Monocyte Chemoattractant Protein-1; MIP-α/β, Macrophage Inflammatory Protein-1 alpha/beta; MMP-3, Matrix metalloproteinase-3; MMP-9, Matrix metalloproteinase-9; and NGAL, Neutrophil gelatinase-associated lipocalin. All data presented as mean±SEM. Statistical significance was determined via two-way ANOVA with Tukey’s multiple comparison test for B-C and via two-tailed T-test for E-G, I, and L-N (*P<0.05).

    Article Snippet: Cardiac cytokine profiling was conducted using the Proteome Profiler Mouse XL Cytokine Array Kit (R&D Systems, Cat. No. ARY028) as previously described.

    Techniques: In Vivo, Comparison, Two Tailed Test