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protein profile array  (R&D Systems)


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    R&D Systems protein profile array
    Protein Profile Array, supplied by R&D Systems, used in various techniques. Bioz Stars score: 97/100, based on 751 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/protein profile array/product/R&D Systems
    Average 97 stars, based on 751 article reviews
    protein profile array - by Bioz Stars, 2026-02
    97/100 stars

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    The impact of E2F1 on immune cell infiltration and <t>cytokine</t> release in coculture with T cells. (A, B) Correlation of E2F1 expression with infiltration of monocytes, eosinophils, and neutrophils in melanoma patients with primary tumors (A) or metastasis (B) . (C, D) Estimation of CD4 + Th1 and Th2 cell infiltration cells in melanoma patients with primary tumors or metastasis correlated to the expression of E2F1, IL-6 (C) , and STAT3, CD274 (D) . Significant correlations are highlighted in red. (E, F) Cytokine assays of supernatants from different culture/coculture conditions were compared as illustrated showing an E2F1-dependent increased secretion of immunosuppressive type 2 cytokines (E) that was completely reversed after E2F1-KD in melanoma cells (F) . Asterisks indicate transcriptionally upregulated factors. FC, fold change.
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    The impact of E2F1 on immune cell infiltration and cytokine release in coculture with T cells. (A, B) Correlation of E2F1 expression with infiltration of monocytes, eosinophils, and neutrophils in melanoma patients with primary tumors (A) or metastasis (B) . (C, D) Estimation of CD4 + Th1 and Th2 cell infiltration cells in melanoma patients with primary tumors or metastasis correlated to the expression of E2F1, IL-6 (C) , and STAT3, CD274 (D) . Significant correlations are highlighted in red. (E, F) Cytokine assays of supernatants from different culture/coculture conditions were compared as illustrated showing an E2F1-dependent increased secretion of immunosuppressive type 2 cytokines (E) that was completely reversed after E2F1-KD in melanoma cells (F) . Asterisks indicate transcriptionally upregulated factors. FC, fold change.

    Journal: Frontiers in Immunology

    Article Title: E2F1-induced autocrine IL-6 inflammatory loop mediates cancer-immune crosstalk that predicts T cell phenotype switching and therapeutic responsiveness

    doi: 10.3389/fimmu.2024.1470368

    Figure Lengend Snippet: The impact of E2F1 on immune cell infiltration and cytokine release in coculture with T cells. (A, B) Correlation of E2F1 expression with infiltration of monocytes, eosinophils, and neutrophils in melanoma patients with primary tumors (A) or metastasis (B) . (C, D) Estimation of CD4 + Th1 and Th2 cell infiltration cells in melanoma patients with primary tumors or metastasis correlated to the expression of E2F1, IL-6 (C) , and STAT3, CD274 (D) . Significant correlations are highlighted in red. (E, F) Cytokine assays of supernatants from different culture/coculture conditions were compared as illustrated showing an E2F1-dependent increased secretion of immunosuppressive type 2 cytokines (E) that was completely reversed after E2F1-KD in melanoma cells (F) . Asterisks indicate transcriptionally upregulated factors. FC, fold change.

    Article Snippet: To measure secreted proteins Proteome Profiler Human Cytokine Array Kit was used according to manufacturer’s instruction (#ARY005B, R&D Systems).

    Techniques: Expressing

    Mathematical model and overview of the melanoma-CD4 + T cell crosstalk with E2F1-STAT3/IL-6/IL6R axis. (A) Mathematical model of the E2F1-STAT3/IL-6 axis including the auto- and paracrine feedback loops from melanoma and immune cells. The heatmap shows that factors related to the IL6R-STAT3-E2F1 pathway are expressed in melanoma and CD4 + T cells prior to activation and crosstalk. (B) Crosstalk simulation illustrating IL-6 expression in melanoma and CD4 + T cells. (C) Output of simulation representing expression levels of E2F1 or STAT3 that are sufficient to trigger IL-6 secretion in melanoma cells. (D) The impact from E2F1 on the melanoma T cell crosstalk where high E2F1 expression leads to an immunosuppressive TME through feedback loops triggered increased release of IL-6 inducing a Th2 shift (left). In contrast, E2F1 depletion in melanoma cells blocks the augmented IL-6 secretion and, in turn, diminishes type-2 cytokine production favoring an anti-tumor Th1 response.

    Journal: Frontiers in Immunology

    Article Title: E2F1-induced autocrine IL-6 inflammatory loop mediates cancer-immune crosstalk that predicts T cell phenotype switching and therapeutic responsiveness

    doi: 10.3389/fimmu.2024.1470368

    Figure Lengend Snippet: Mathematical model and overview of the melanoma-CD4 + T cell crosstalk with E2F1-STAT3/IL-6/IL6R axis. (A) Mathematical model of the E2F1-STAT3/IL-6 axis including the auto- and paracrine feedback loops from melanoma and immune cells. The heatmap shows that factors related to the IL6R-STAT3-E2F1 pathway are expressed in melanoma and CD4 + T cells prior to activation and crosstalk. (B) Crosstalk simulation illustrating IL-6 expression in melanoma and CD4 + T cells. (C) Output of simulation representing expression levels of E2F1 or STAT3 that are sufficient to trigger IL-6 secretion in melanoma cells. (D) The impact from E2F1 on the melanoma T cell crosstalk where high E2F1 expression leads to an immunosuppressive TME through feedback loops triggered increased release of IL-6 inducing a Th2 shift (left). In contrast, E2F1 depletion in melanoma cells blocks the augmented IL-6 secretion and, in turn, diminishes type-2 cytokine production favoring an anti-tumor Th1 response.

    Article Snippet: To measure secreted proteins Proteome Profiler Human Cytokine Array Kit was used according to manufacturer’s instruction (#ARY005B, R&D Systems).

    Techniques: Activation Assay, Expressing