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mitobright ros deep red  (Dojindo Labs)


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    Dojindo Labs mitobright ros deep red
    (A) Schematic overview of the experimental workflow and timeline for genetic (siRNA-mediated knockdown) and pharmacological (AZD3965) inhibition of MCT1 in AC16 cardiomyocytes-derived cells under hypoxic conditions. (B, C) Immunoblot analysis of lysine lactylation on PDK1 (B) and PDK2 (C) following immunoprecipitation from AC16 cells under normoxic or hypoxic conditions with or without MCT1 knockdown or AZD3965 treatment. (D) Quantification of PDK1 and PDK2 lactylation normalized to immunoprecipitated protein levels. (E) Representative immunoblot showing p-PDH levels in AC16 cells subjected to hypoxia with genetic or pharmacological inhibition of MCT1. (F) Quantification of p-PDH protein levels. (G) Representative confocal images showing mitochondrial <t>ROS</t> generation detected using <t>MitoBright</t> ROS Deep Red (MBR Deep Red) in hypoxic AC16 cells with MCT1 knockdown or AZD3965 treatment. (H) Quantification of mitochondrial ROS fluorescence intensity. Scale bar, 20 µm; magnification, 60x. (I) Schematic summary illustrating MCT1-dependent modulation of mitochondrial lactylation, PDH regulation, and mitochondrial function under hypoxic conditions in AC16 cells. Data are presented as mean ± SEM from n = 3–6 independent experiments. Statistical significance was determined by one-way ANOVA with Tukey’s multiple-comparisons test. P < 0.05, P < 0.01, P < 0.001, P < 0.0001.
    Mitobright Ros Deep Red, supplied by Dojindo Labs, used in various techniques. Bioz Stars score: 94/100, based on 36 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mitobright+ros+deep+red/MitoBright+ROS+Deep+Red+-+Mitochondrial+Superoxide+Detection/bio_rxiv__64898__2026__04__27__718938-121-23-30
    Average 94 stars, based on 36 article reviews
    mitobright ros deep red - by Bioz Stars, 2026-10
    94/100 stars

    Images

    1) Product Images from "Lactylation landscape of mitochondrial proteins in myocardial infarction"

    Article Title: Lactylation landscape of mitochondrial proteins in myocardial infarction

    Journal: bioRxiv

    doi: 10.64898/2026.04.27.718938

    (A) Schematic overview of the experimental workflow and timeline for genetic (siRNA-mediated knockdown) and pharmacological (AZD3965) inhibition of MCT1 in AC16 cardiomyocytes-derived cells under hypoxic conditions. (B, C) Immunoblot analysis of lysine lactylation on PDK1 (B) and PDK2 (C) following immunoprecipitation from AC16 cells under normoxic or hypoxic conditions with or without MCT1 knockdown or AZD3965 treatment. (D) Quantification of PDK1 and PDK2 lactylation normalized to immunoprecipitated protein levels. (E) Representative immunoblot showing p-PDH levels in AC16 cells subjected to hypoxia with genetic or pharmacological inhibition of MCT1. (F) Quantification of p-PDH protein levels. (G) Representative confocal images showing mitochondrial ROS generation detected using MitoBright ROS Deep Red (MBR Deep Red) in hypoxic AC16 cells with MCT1 knockdown or AZD3965 treatment. (H) Quantification of mitochondrial ROS fluorescence intensity. Scale bar, 20 µm; magnification, 60x. (I) Schematic summary illustrating MCT1-dependent modulation of mitochondrial lactylation, PDH regulation, and mitochondrial function under hypoxic conditions in AC16 cells. Data are presented as mean ± SEM from n = 3–6 independent experiments. Statistical significance was determined by one-way ANOVA with Tukey’s multiple-comparisons test. P < 0.05, P < 0.01, P < 0.001, P < 0.0001.
    Figure Legend Snippet: (A) Schematic overview of the experimental workflow and timeline for genetic (siRNA-mediated knockdown) and pharmacological (AZD3965) inhibition of MCT1 in AC16 cardiomyocytes-derived cells under hypoxic conditions. (B, C) Immunoblot analysis of lysine lactylation on PDK1 (B) and PDK2 (C) following immunoprecipitation from AC16 cells under normoxic or hypoxic conditions with or without MCT1 knockdown or AZD3965 treatment. (D) Quantification of PDK1 and PDK2 lactylation normalized to immunoprecipitated protein levels. (E) Representative immunoblot showing p-PDH levels in AC16 cells subjected to hypoxia with genetic or pharmacological inhibition of MCT1. (F) Quantification of p-PDH protein levels. (G) Representative confocal images showing mitochondrial ROS generation detected using MitoBright ROS Deep Red (MBR Deep Red) in hypoxic AC16 cells with MCT1 knockdown or AZD3965 treatment. (H) Quantification of mitochondrial ROS fluorescence intensity. Scale bar, 20 µm; magnification, 60x. (I) Schematic summary illustrating MCT1-dependent modulation of mitochondrial lactylation, PDH regulation, and mitochondrial function under hypoxic conditions in AC16 cells. Data are presented as mean ± SEM from n = 3–6 independent experiments. Statistical significance was determined by one-way ANOVA with Tukey’s multiple-comparisons test. P < 0.05, P < 0.01, P < 0.001, P < 0.0001.

    Techniques Used: Knockdown, Inhibition, Derivative Assay, Western Blot, Immunoprecipitation, Fluorescence

    Related Articles

    Expressing:

    Article Title: CRTAC1 derived from senescent FLSs induces chondrocyte mitochondrial dysfunction via modulating NRF2/SIRT3 axis in osteoarthritis progression
    Article Snippet: .. The expression of ROS was detected by ROS Assay Kit -Highly Sensitive DCFH-DA and MitoBright ROS Deep Red (Dojindo, Shanghai, China). ..

    ROS Assay:

    Article Title: CRTAC1 derived from senescent FLSs induces chondrocyte mitochondrial dysfunction via modulating NRF2/SIRT3 axis in osteoarthritis progression
    Article Snippet: .. The expression of ROS was detected by ROS Assay Kit -Highly Sensitive DCFH-DA and MitoBright ROS Deep Red (Dojindo, Shanghai, China). ..

    Fluorescence:

    Article Title: Lactylation landscape of mitochondrial proteins in myocardial infarction
    Article Snippet: .. To measure mitochondrial ROS, AC16 cells (2□×□10 5 ) were seeded in MatTek collagen-coated glass-bottom 35 mm culture plates and loaded with 5□μM MitoBright ROS Deep Red (MBR Deep Red) (Dojindo Molecular Technologies, CatMT16-12) for 30□min at 37□°C, and measured the fluorescence at 540/ex and 670/em using an Olympus Evident FV4000 Confocal Microscope (Olympus) using a 60x oil objective. .. The images were quantified as mean fluorescence intensity per cell using ImageJ software, ensuring consistent thresholding and background subtraction across all samples.

    Microscopy:

    Article Title: Lactylation landscape of mitochondrial proteins in myocardial infarction
    Article Snippet: .. To measure mitochondrial ROS, AC16 cells (2□×□10 5 ) were seeded in MatTek collagen-coated glass-bottom 35 mm culture plates and loaded with 5□μM MitoBright ROS Deep Red (MBR Deep Red) (Dojindo Molecular Technologies, CatMT16-12) for 30□min at 37□°C, and measured the fluorescence at 540/ex and 670/em using an Olympus Evident FV4000 Confocal Microscope (Olympus) using a 60x oil objective. .. The images were quantified as mean fluorescence intensity per cell using ImageJ software, ensuring consistent thresholding and background subtraction across all samples.

    other:

    Article Title: Physiological medium and 3-hydroxybutyrate modulate autophagy-linked organelle remodeling in human external urethral sphincter myoblasts
    Article Snippet: Mitochondrial superoxide levels were detected using MitoBright ROS Deep Red (MT-1,Dojindo Laboratories, Kumamoto, Japan).



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    (A) Schematic overview of the experimental workflow and timeline for genetic (siRNA-mediated knockdown) and pharmacological (AZD3965) inhibition of MCT1 in AC16 cardiomyocytes-derived cells under hypoxic conditions. (B, C) Immunoblot analysis of lysine lactylation on PDK1 (B) and PDK2 (C) following immunoprecipitation from AC16 cells under normoxic or hypoxic conditions with or without MCT1 knockdown or AZD3965 treatment. (D) Quantification of PDK1 and PDK2 lactylation normalized to immunoprecipitated protein levels. (E) Representative immunoblot showing p-PDH levels in AC16 cells subjected to hypoxia with genetic or pharmacological inhibition of MCT1. (F) Quantification of p-PDH protein levels. (G) Representative confocal images showing mitochondrial <t>ROS</t> generation detected using <t>MitoBright</t> ROS Deep Red (MBR Deep Red) in hypoxic AC16 cells with MCT1 knockdown or AZD3965 treatment. (H) Quantification of mitochondrial ROS fluorescence intensity. Scale bar, 20 µm; magnification, 60x. (I) Schematic summary illustrating MCT1-dependent modulation of mitochondrial lactylation, PDH regulation, and mitochondrial function under hypoxic conditions in AC16 cells. Data are presented as mean ± SEM from n = 3–6 independent experiments. Statistical significance was determined by one-way ANOVA with Tukey’s multiple-comparisons test. P < 0.05, P < 0.01, P < 0.001, P < 0.0001.
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    (A) Schematic overview of the experimental workflow and timeline for genetic (siRNA-mediated knockdown) and pharmacological (AZD3965) inhibition of MCT1 in AC16 cardiomyocytes-derived cells under hypoxic conditions. (B, C) Immunoblot analysis of lysine lactylation on PDK1 (B) and PDK2 (C) following immunoprecipitation from AC16 cells under normoxic or hypoxic conditions with or without MCT1 knockdown or AZD3965 treatment. (D) Quantification of PDK1 and PDK2 lactylation normalized to immunoprecipitated protein levels. (E) Representative immunoblot showing p-PDH levels in AC16 cells subjected to hypoxia with genetic or pharmacological inhibition of MCT1. (F) Quantification of p-PDH protein levels. (G) Representative confocal images showing mitochondrial <t>ROS</t> generation detected using <t>MitoBright</t> ROS Deep Red (MBR Deep Red) in hypoxic AC16 cells with MCT1 knockdown or AZD3965 treatment. (H) Quantification of mitochondrial ROS fluorescence intensity. Scale bar, 20 µm; magnification, 60x. (I) Schematic summary illustrating MCT1-dependent modulation of mitochondrial lactylation, PDH regulation, and mitochondrial function under hypoxic conditions in AC16 cells. Data are presented as mean ± SEM from n = 3–6 independent experiments. Statistical significance was determined by one-way ANOVA with Tukey’s multiple-comparisons test. P < 0.05, P < 0.01, P < 0.001, P < 0.0001.
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    (A) Schematic overview of the experimental workflow and timeline for genetic (siRNA-mediated knockdown) and pharmacological (AZD3965) inhibition of MCT1 in AC16 cardiomyocytes-derived cells under hypoxic conditions. (B, C) Immunoblot analysis of lysine lactylation on PDK1 (B) and PDK2 (C) following immunoprecipitation from AC16 cells under normoxic or hypoxic conditions with or without MCT1 knockdown or AZD3965 treatment. (D) Quantification of PDK1 and PDK2 lactylation normalized to immunoprecipitated protein levels. (E) Representative immunoblot showing p-PDH levels in AC16 cells subjected to hypoxia with genetic or pharmacological inhibition of MCT1. (F) Quantification of p-PDH protein levels. (G) Representative confocal images showing mitochondrial <t>ROS</t> generation detected using <t>MitoBright</t> ROS Deep Red (MBR Deep Red) in hypoxic AC16 cells with MCT1 knockdown or AZD3965 treatment. (H) Quantification of mitochondrial ROS fluorescence intensity. Scale bar, 20 µm; magnification, 60x. (I) Schematic summary illustrating MCT1-dependent modulation of mitochondrial lactylation, PDH regulation, and mitochondrial function under hypoxic conditions in AC16 cells. Data are presented as mean ± SEM from n = 3–6 independent experiments. Statistical significance was determined by one-way ANOVA with Tukey’s multiple-comparisons test. P < 0.05, P < 0.01, P < 0.001, P < 0.0001.
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    Image Search Results


    (A) Schematic overview of the experimental workflow and timeline for genetic (siRNA-mediated knockdown) and pharmacological (AZD3965) inhibition of MCT1 in AC16 cardiomyocytes-derived cells under hypoxic conditions. (B, C) Immunoblot analysis of lysine lactylation on PDK1 (B) and PDK2 (C) following immunoprecipitation from AC16 cells under normoxic or hypoxic conditions with or without MCT1 knockdown or AZD3965 treatment. (D) Quantification of PDK1 and PDK2 lactylation normalized to immunoprecipitated protein levels. (E) Representative immunoblot showing p-PDH levels in AC16 cells subjected to hypoxia with genetic or pharmacological inhibition of MCT1. (F) Quantification of p-PDH protein levels. (G) Representative confocal images showing mitochondrial ROS generation detected using MitoBright ROS Deep Red (MBR Deep Red) in hypoxic AC16 cells with MCT1 knockdown or AZD3965 treatment. (H) Quantification of mitochondrial ROS fluorescence intensity. Scale bar, 20 µm; magnification, 60x. (I) Schematic summary illustrating MCT1-dependent modulation of mitochondrial lactylation, PDH regulation, and mitochondrial function under hypoxic conditions in AC16 cells. Data are presented as mean ± SEM from n = 3–6 independent experiments. Statistical significance was determined by one-way ANOVA with Tukey’s multiple-comparisons test. P < 0.05, P < 0.01, P < 0.001, P < 0.0001.

    Journal: bioRxiv

    Article Title: Lactylation landscape of mitochondrial proteins in myocardial infarction

    doi: 10.64898/2026.04.27.718938

    Figure Lengend Snippet: (A) Schematic overview of the experimental workflow and timeline for genetic (siRNA-mediated knockdown) and pharmacological (AZD3965) inhibition of MCT1 in AC16 cardiomyocytes-derived cells under hypoxic conditions. (B, C) Immunoblot analysis of lysine lactylation on PDK1 (B) and PDK2 (C) following immunoprecipitation from AC16 cells under normoxic or hypoxic conditions with or without MCT1 knockdown or AZD3965 treatment. (D) Quantification of PDK1 and PDK2 lactylation normalized to immunoprecipitated protein levels. (E) Representative immunoblot showing p-PDH levels in AC16 cells subjected to hypoxia with genetic or pharmacological inhibition of MCT1. (F) Quantification of p-PDH protein levels. (G) Representative confocal images showing mitochondrial ROS generation detected using MitoBright ROS Deep Red (MBR Deep Red) in hypoxic AC16 cells with MCT1 knockdown or AZD3965 treatment. (H) Quantification of mitochondrial ROS fluorescence intensity. Scale bar, 20 µm; magnification, 60x. (I) Schematic summary illustrating MCT1-dependent modulation of mitochondrial lactylation, PDH regulation, and mitochondrial function under hypoxic conditions in AC16 cells. Data are presented as mean ± SEM from n = 3–6 independent experiments. Statistical significance was determined by one-way ANOVA with Tukey’s multiple-comparisons test. P < 0.05, P < 0.01, P < 0.001, P < 0.0001.

    Article Snippet: To measure mitochondrial ROS, AC16 cells (2□×□10 5 ) were seeded in MatTek collagen-coated glass-bottom 35 mm culture plates and loaded with 5□μM MitoBright ROS Deep Red (MBR Deep Red) (Dojindo Molecular Technologies, Cat#MT16-12) for 30□min at 37□°C, and measured the fluorescence at 540/ex and 670/em using an Olympus Evident FV4000 Confocal Microscope (Olympus) using a 60x oil objective.

    Techniques: Knockdown, Inhibition, Derivative Assay, Western Blot, Immunoprecipitation, Fluorescence