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rapid taq master mix  (Vazyme Biotech Co)


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    Vazyme Biotech Co rapid taq master mix
    Rapid Taq Master Mix, supplied by Vazyme Biotech Co, used in various techniques. Bioz Stars score: 99/100, based on 605 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rapid taq master mix/product/Vazyme Biotech Co
    Average 99 stars, based on 605 article reviews
    rapid taq master mix - by Bioz Stars, 2026-02
    99/100 stars

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    In vitro evaluation of immunomodulatory effects in composite hydrogel systems involving Nnat . (A) Top: Schematic representation of in vitro inflammatory model; Bottom: Morphological changes in macrophages observed via light microscopy. Scale bars: 100 μm. (B) Flow cytometric analysis of reactive oxygen species. (C) Phenotypic characterization of macrophage subtypes (M0/M1/M2) through surface marker detection. (D) Enhanced activation of NF-κB/P38 signaling pathways with elevated PI3K phosphorylation observed in Hydrogel + si- Nnat group versus hydrogel control. (E) <t>Quantitative</t> <t>PCR</t> analysis of gene expression. (F) Metabolic activity assessment through viability assays. (G) Apoptotic cell quantification. (H) TUNEL staining patterns across experimental groups. Scale bars: 50 μm. (I) Cytokine profile analysis using ELISA. (n = 5, ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001.)
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    In vitro evaluation of immunomodulatory effects in composite hydrogel systems involving Nnat . (A) Top: Schematic representation of in vitro inflammatory model; Bottom: Morphological changes in macrophages observed via light microscopy. Scale bars: 100 μm. (B) Flow cytometric analysis of reactive oxygen species. (C) Phenotypic characterization of macrophage subtypes (M0/M1/M2) through surface marker detection. (D) Enhanced activation of NF-κB/P38 signaling pathways with elevated PI3K phosphorylation observed in Hydrogel + si- Nnat group versus hydrogel control. (E) <t>Quantitative</t> <t>PCR</t> analysis of gene expression. (F) Metabolic activity assessment through viability assays. (G) Apoptotic cell quantification. (H) TUNEL staining patterns across experimental groups. Scale bars: 50 μm. (I) Cytokine profile analysis using ELISA. (n = 5, ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001.)
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    In vitro evaluation of immunomodulatory effects in composite hydrogel systems involving Nnat . (A) Top: Schematic representation of in vitro inflammatory model; Bottom: Morphological changes in macrophages observed via light microscopy. Scale bars: 100 μm. (B) Flow cytometric analysis of reactive oxygen species. (C) Phenotypic characterization of macrophage subtypes (M0/M1/M2) through surface marker detection. (D) Enhanced activation of NF-κB/P38 signaling pathways with elevated PI3K phosphorylation observed in Hydrogel + si- Nnat group versus hydrogel control. (E) <t>Quantitative</t> <t>PCR</t> analysis of gene expression. (F) Metabolic activity assessment through viability assays. (G) Apoptotic cell quantification. (H) TUNEL staining patterns across experimental groups. Scale bars: 50 μm. (I) Cytokine profile analysis using ELISA. (n = 5, ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001.)
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    In vitro evaluation of immunomodulatory effects in composite hydrogel systems involving Nnat . (A) Top: Schematic representation of in vitro inflammatory model; Bottom: Morphological changes in macrophages observed via light microscopy. Scale bars: 100 μm. (B) Flow cytometric analysis of reactive oxygen species. (C) Phenotypic characterization of macrophage subtypes (M0/M1/M2) through surface marker detection. (D) Enhanced activation of NF-κB/P38 signaling pathways with elevated PI3K phosphorylation observed in Hydrogel + si- Nnat group versus hydrogel control. (E) <t>Quantitative</t> <t>PCR</t> analysis of gene expression. (F) Metabolic activity assessment through viability assays. (G) Apoptotic cell quantification. (H) TUNEL staining patterns across experimental groups. Scale bars: 50 μm. (I) Cytokine profile analysis using ELISA. (n = 5, ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001.)
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    In vitro evaluation of immunomodulatory effects in composite hydrogel systems involving Nnat . (A) Top: Schematic representation of in vitro inflammatory model; Bottom: Morphological changes in macrophages observed via light microscopy. Scale bars: 100 μm. (B) Flow cytometric analysis of reactive oxygen species. (C) Phenotypic characterization of macrophage subtypes (M0/M1/M2) through surface marker detection. (D) Enhanced activation of NF-κB/P38 signaling pathways with elevated PI3K phosphorylation observed in Hydrogel + si- Nnat group versus hydrogel control. (E) <t>Quantitative</t> <t>PCR</t> analysis of gene expression. (F) Metabolic activity assessment through viability assays. (G) Apoptotic cell quantification. (H) TUNEL staining patterns across experimental groups. Scale bars: 50 μm. (I) Cytokine profile analysis using ELISA. (n = 5, ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001.)
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    MSLN and D1 domain promote ovarian cancer cell migration and invasion through the AKT-MMP7 signaling pathway Wound-healing assays showing migration of OVCAR3 MSLN KO (A) and SKOV3 (B) cells after 48 h treatment with MSLN-Fc, D1-Fc, D2-Fc, D3-Fc, or Fc. Data were normalized to the PBS group. Invasion assays of OVCAR3 MSLN KO (C) and SKOV3 (D) cells under the same treatment conditions for 48 h. <t>RT-qPCR</t> analysis of Mmp7 and Mmp9 mRNA expression in response to MSLN-Fc stimulation over time (E) and at increasing concentrations (F). Western blot showing MMP7 protein expression induced by escalating doses of MSLN-Fc, with Fc as control (G). Western blot analysis of MMP7, E-cadherin, and AKT phosphorylation in OVCAR3 MSLN KO (H) and SKOV3 (I) cells treated for 24 h with 100 nM MSLN-Fc, D1-Fc, D2-Fc, D3-Fc, or Fc. All quantitative data are presented as mean ± SD from three biologically independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001; data were analyzed by ANOVA followed by Tukey’s multiple comparison test.
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    New England Biolabs taq 2× master mix
    MSLN and D1 domain promote ovarian cancer cell migration and invasion through the AKT-MMP7 signaling pathway Wound-healing assays showing migration of OVCAR3 MSLN KO (A) and SKOV3 (B) cells after 48 h treatment with MSLN-Fc, D1-Fc, D2-Fc, D3-Fc, or Fc. Data were normalized to the PBS group. Invasion assays of OVCAR3 MSLN KO (C) and SKOV3 (D) cells under the same treatment conditions for 48 h. <t>RT-qPCR</t> analysis of Mmp7 and Mmp9 mRNA expression in response to MSLN-Fc stimulation over time (E) and at increasing concentrations (F). Western blot showing MMP7 protein expression induced by escalating doses of MSLN-Fc, with Fc as control (G). Western blot analysis of MMP7, E-cadherin, and AKT phosphorylation in OVCAR3 MSLN KO (H) and SKOV3 (I) cells treated for 24 h with 100 nM MSLN-Fc, D1-Fc, D2-Fc, D3-Fc, or Fc. All quantitative data are presented as mean ± SD from three biologically independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001; data were analyzed by ANOVA followed by Tukey’s multiple comparison test.
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    Image Search Results


    In vitro evaluation of immunomodulatory effects in composite hydrogel systems involving Nnat . (A) Top: Schematic representation of in vitro inflammatory model; Bottom: Morphological changes in macrophages observed via light microscopy. Scale bars: 100 μm. (B) Flow cytometric analysis of reactive oxygen species. (C) Phenotypic characterization of macrophage subtypes (M0/M1/M2) through surface marker detection. (D) Enhanced activation of NF-κB/P38 signaling pathways with elevated PI3K phosphorylation observed in Hydrogel + si- Nnat group versus hydrogel control. (E) Quantitative PCR analysis of gene expression. (F) Metabolic activity assessment through viability assays. (G) Apoptotic cell quantification. (H) TUNEL staining patterns across experimental groups. Scale bars: 50 μm. (I) Cytokine profile analysis using ELISA. (n = 5, ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001.)

    Journal: Bioactive Materials

    Article Title: Exosome-functionalized photocrosslinked GelMA/HAMA hydrogel promotes facial nerve recovery via inflammatory microenvironment regulation

    doi: 10.1016/j.bioactmat.2026.01.008

    Figure Lengend Snippet: In vitro evaluation of immunomodulatory effects in composite hydrogel systems involving Nnat . (A) Top: Schematic representation of in vitro inflammatory model; Bottom: Morphological changes in macrophages observed via light microscopy. Scale bars: 100 μm. (B) Flow cytometric analysis of reactive oxygen species. (C) Phenotypic characterization of macrophage subtypes (M0/M1/M2) through surface marker detection. (D) Enhanced activation of NF-κB/P38 signaling pathways with elevated PI3K phosphorylation observed in Hydrogel + si- Nnat group versus hydrogel control. (E) Quantitative PCR analysis of gene expression. (F) Metabolic activity assessment through viability assays. (G) Apoptotic cell quantification. (H) TUNEL staining patterns across experimental groups. Scale bars: 50 μm. (I) Cytokine profile analysis using ELISA. (n = 5, ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001.)

    Article Snippet: Reaction systems (20 μL volume) were assembled in RNase-free tubes, incorporating cDNA templates, paired forward/reverse primers (10 μM concentration per primer), Vazyme's 2 × Taq Pro Universal SYBR qPCR Master Mix, and molecular-grade water.

    Techniques: In Vitro, Light Microscopy, Marker, Activation Assay, Protein-Protein interactions, Phospho-proteomics, Control, Real-time Polymerase Chain Reaction, Gene Expression, Activity Assay, TUNEL Assay, Staining, Enzyme-linked Immunosorbent Assay

    MSLN and D1 domain promote ovarian cancer cell migration and invasion through the AKT-MMP7 signaling pathway Wound-healing assays showing migration of OVCAR3 MSLN KO (A) and SKOV3 (B) cells after 48 h treatment with MSLN-Fc, D1-Fc, D2-Fc, D3-Fc, or Fc. Data were normalized to the PBS group. Invasion assays of OVCAR3 MSLN KO (C) and SKOV3 (D) cells under the same treatment conditions for 48 h. RT-qPCR analysis of Mmp7 and Mmp9 mRNA expression in response to MSLN-Fc stimulation over time (E) and at increasing concentrations (F). Western blot showing MMP7 protein expression induced by escalating doses of MSLN-Fc, with Fc as control (G). Western blot analysis of MMP7, E-cadherin, and AKT phosphorylation in OVCAR3 MSLN KO (H) and SKOV3 (I) cells treated for 24 h with 100 nM MSLN-Fc, D1-Fc, D2-Fc, D3-Fc, or Fc. All quantitative data are presented as mean ± SD from three biologically independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001; data were analyzed by ANOVA followed by Tukey’s multiple comparison test.

    Journal: Molecular Therapy Oncology

    Article Title: A monoclonal antibody W1 blocks mesothelin-mediated tumor progression

    doi: 10.1016/j.omton.2025.201094

    Figure Lengend Snippet: MSLN and D1 domain promote ovarian cancer cell migration and invasion through the AKT-MMP7 signaling pathway Wound-healing assays showing migration of OVCAR3 MSLN KO (A) and SKOV3 (B) cells after 48 h treatment with MSLN-Fc, D1-Fc, D2-Fc, D3-Fc, or Fc. Data were normalized to the PBS group. Invasion assays of OVCAR3 MSLN KO (C) and SKOV3 (D) cells under the same treatment conditions for 48 h. RT-qPCR analysis of Mmp7 and Mmp9 mRNA expression in response to MSLN-Fc stimulation over time (E) and at increasing concentrations (F). Western blot showing MMP7 protein expression induced by escalating doses of MSLN-Fc, with Fc as control (G). Western blot analysis of MMP7, E-cadherin, and AKT phosphorylation in OVCAR3 MSLN KO (H) and SKOV3 (I) cells treated for 24 h with 100 nM MSLN-Fc, D1-Fc, D2-Fc, D3-Fc, or Fc. All quantitative data are presented as mean ± SD from three biologically independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001; data were analyzed by ANOVA followed by Tukey’s multiple comparison test.

    Article Snippet: Subsequently, qPCR was conducted using Taq Pro Universal SYBR qPCR Master Mix (Vazyme, cat#Q712-02).

    Techniques: Migration, Quantitative RT-PCR, Expressing, Western Blot, Control, Phospho-proteomics, Comparison

    W1 mIgG1 inhibits ovarian cancer cell migration and invasion in a dose-dependent manner by downregulating MMP7 (A) Wound-healing assay showing the migration of OVCAR3 cells treated with increasing concentrations of W1 mIgG1 (100, 300, 600 nM). Data were normalized to the PBS group. (B) Transwell invasion assay demonstrating the dose-dependent suppression of OVCAR3 cell invasion by W1 mIgG1. RT-qPCR (C) and Western blot (D) analyses revealed that W1 mIgG1 treatment progressively reduced Mmp7 expression at both mRNA and protein levels in OVCAR3 cells, whereas A12H cIgG1 (300 nM) showed no effect. Comparative effects of W1 mIgG1 (300 nM) and the MMPi (1,000 nM) on MSLN-induced cell migration (E) and invasion (F). Both treatments showed similar inhibitory efficacy. All quantitative data are presented as mean ± SD from three biologically independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001; data were analyzed by ANOVA followed by Tukey’s multiple comparison test.

    Journal: Molecular Therapy Oncology

    Article Title: A monoclonal antibody W1 blocks mesothelin-mediated tumor progression

    doi: 10.1016/j.omton.2025.201094

    Figure Lengend Snippet: W1 mIgG1 inhibits ovarian cancer cell migration and invasion in a dose-dependent manner by downregulating MMP7 (A) Wound-healing assay showing the migration of OVCAR3 cells treated with increasing concentrations of W1 mIgG1 (100, 300, 600 nM). Data were normalized to the PBS group. (B) Transwell invasion assay demonstrating the dose-dependent suppression of OVCAR3 cell invasion by W1 mIgG1. RT-qPCR (C) and Western blot (D) analyses revealed that W1 mIgG1 treatment progressively reduced Mmp7 expression at both mRNA and protein levels in OVCAR3 cells, whereas A12H cIgG1 (300 nM) showed no effect. Comparative effects of W1 mIgG1 (300 nM) and the MMPi (1,000 nM) on MSLN-induced cell migration (E) and invasion (F). Both treatments showed similar inhibitory efficacy. All quantitative data are presented as mean ± SD from three biologically independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001; data were analyzed by ANOVA followed by Tukey’s multiple comparison test.

    Article Snippet: Subsequently, qPCR was conducted using Taq Pro Universal SYBR qPCR Master Mix (Vazyme, cat#Q712-02).

    Techniques: Migration, Wound Healing Assay, Transwell Invasion Assay, Quantitative RT-PCR, Western Blot, Expressing, Comparison