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glut1 inhibitor bay876  (MedChemExpress)


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    MedChemExpress glut1 inhibitor bay876
    Glut1 Inhibitor Bay876, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 63 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 95 stars, based on 63 article reviews
    glut1 inhibitor bay876 - by Bioz Stars, 2026-02
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    Adooq Bioscience LLC glut1 inhibitor bay876
    Fold change difference between 50% and 100% confluence of GLUT mRNA expression in OKF6 and oral squamous cell carcinoma cells when treated with <t>BAY876</t> or WZB117. Each data point was obtained from 3 biological replicates and error bars represent the SD. The control was baseline expression with no inhibitor present and the SD is an averaged SD from all groups.
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    Millipore glut1 inhibitor bay876
    Glucose uptake and <t>GLUT1</t> expression in HUVECs under normoxia and hypoxia. a Glucose uptake of HUVECs under normoxia and hypoxia. HUVECs were exposed to hypoxia, and glucose uptake was measured as described in the Materials and methods. Data are expressed as the mean ± SEM from 6 independent experiments. * P < 0.05 (Mann–Whitney test). b GLUT1 and GLUT3 expression in HUVECs under normoxia and hypoxia determined by immunoblotting. Data are expressed as the mean ± SEM of 12 samples from 3 independent experiments. * P < 0.01 vs. normoxia control of each condition (Mann–Whitney test). c Effect of the GLUT1 inhibitor <t>BAY876</t> on glucose uptake in HUVECs. HUVECs were cultured under normoxia or hypoxia with BAY876 as described in the Materials and Methods. Data are expressed as a percentage of glucose uptake compared with vehicle control in each condition. Data are expressed as the mean ± SEM from 5 independent results. * P < 0.01 (one-way ANOVA). d Effect of GLUT1 inhibitor on sprouting of cells from choroid explants . The explants were treated with vehicle or the GLUT1 inhibitor BAY876 for 4 days. Images were taken and the area of cell sprouting was quantified by ImageJ software. Data are the mean ± SEM from 12 explants in 2 time-independent experiments with similar results. *P < 0.01 (one-way ANOVA with Dunnett’s correction). e GLUT1 expression in HUVECs under normoxia and hypoxia determined by immunoblotting. Data are expressed as the mean ± SEM from 6 independent experiments. Glb, glibenclamide (10 μM). * P < 0.01 vs. normoxia control of each condition (Mann–Whitney test)
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    Image Search Results


    Fold change difference between 50% and 100% confluence of GLUT mRNA expression in OKF6 and oral squamous cell carcinoma cells when treated with BAY876 or WZB117. Each data point was obtained from 3 biological replicates and error bars represent the SD. The control was baseline expression with no inhibitor present and the SD is an averaged SD from all groups.

    Journal: Journal of Oral Pathology & Medicine

    Article Title: Transcriptional regulation of glucose transporters in human oral squamous cell carcinoma cells

    doi: 10.1111/jop.13342

    Figure Lengend Snippet: Fold change difference between 50% and 100% confluence of GLUT mRNA expression in OKF6 and oral squamous cell carcinoma cells when treated with BAY876 or WZB117. Each data point was obtained from 3 biological replicates and error bars represent the SD. The control was baseline expression with no inhibitor present and the SD is an averaged SD from all groups.

    Article Snippet: Cells were treated with 500 nM BAY876 (GLUT1 inhibitor; A17216; ADOOQ Bioscience) and 25 μM WZB117 (GLUT1, GLUT3 and GLUT4 inhibitor; 19900; Cayman Chemical Company) 24 h before they were expected to reach the chosen confluency.

    Techniques: Expressing, Control

    Glucose uptake and GLUT1 expression in HUVECs under normoxia and hypoxia. a Glucose uptake of HUVECs under normoxia and hypoxia. HUVECs were exposed to hypoxia, and glucose uptake was measured as described in the Materials and methods. Data are expressed as the mean ± SEM from 6 independent experiments. * P < 0.05 (Mann–Whitney test). b GLUT1 and GLUT3 expression in HUVECs under normoxia and hypoxia determined by immunoblotting. Data are expressed as the mean ± SEM of 12 samples from 3 independent experiments. * P < 0.01 vs. normoxia control of each condition (Mann–Whitney test). c Effect of the GLUT1 inhibitor BAY876 on glucose uptake in HUVECs. HUVECs were cultured under normoxia or hypoxia with BAY876 as described in the Materials and Methods. Data are expressed as a percentage of glucose uptake compared with vehicle control in each condition. Data are expressed as the mean ± SEM from 5 independent results. * P < 0.01 (one-way ANOVA). d Effect of GLUT1 inhibitor on sprouting of cells from choroid explants . The explants were treated with vehicle or the GLUT1 inhibitor BAY876 for 4 days. Images were taken and the area of cell sprouting was quantified by ImageJ software. Data are the mean ± SEM from 12 explants in 2 time-independent experiments with similar results. *P < 0.01 (one-way ANOVA with Dunnett’s correction). e GLUT1 expression in HUVECs under normoxia and hypoxia determined by immunoblotting. Data are expressed as the mean ± SEM from 6 independent experiments. Glb, glibenclamide (10 μM). * P < 0.01 vs. normoxia control of each condition (Mann–Whitney test)

    Journal: The Journal of Physiological Sciences : JPS

    Article Title: Hypoxia induces the translocation of glucose transporter 1 to the plasma membrane in vascular endothelial cells

    doi: 10.1186/s12576-020-00773-y

    Figure Lengend Snippet: Glucose uptake and GLUT1 expression in HUVECs under normoxia and hypoxia. a Glucose uptake of HUVECs under normoxia and hypoxia. HUVECs were exposed to hypoxia, and glucose uptake was measured as described in the Materials and methods. Data are expressed as the mean ± SEM from 6 independent experiments. * P < 0.05 (Mann–Whitney test). b GLUT1 and GLUT3 expression in HUVECs under normoxia and hypoxia determined by immunoblotting. Data are expressed as the mean ± SEM of 12 samples from 3 independent experiments. * P < 0.01 vs. normoxia control of each condition (Mann–Whitney test). c Effect of the GLUT1 inhibitor BAY876 on glucose uptake in HUVECs. HUVECs were cultured under normoxia or hypoxia with BAY876 as described in the Materials and Methods. Data are expressed as a percentage of glucose uptake compared with vehicle control in each condition. Data are expressed as the mean ± SEM from 5 independent results. * P < 0.01 (one-way ANOVA). d Effect of GLUT1 inhibitor on sprouting of cells from choroid explants . The explants were treated with vehicle or the GLUT1 inhibitor BAY876 for 4 days. Images were taken and the area of cell sprouting was quantified by ImageJ software. Data are the mean ± SEM from 12 explants in 2 time-independent experiments with similar results. *P < 0.01 (one-way ANOVA with Dunnett’s correction). e GLUT1 expression in HUVECs under normoxia and hypoxia determined by immunoblotting. Data are expressed as the mean ± SEM from 6 independent experiments. Glb, glibenclamide (10 μM). * P < 0.01 vs. normoxia control of each condition (Mann–Whitney test)

    Article Snippet: Anti-GLUT3 (PA5-72331) was obtained from Thermo Fisher (Waltham, MA). β-actin antibody (AC-74), ATP-sensitive potassium (KATP) channel inhibitor glibenclamide, mitochondrial KATP channel inhibitor 5-HD, ATP inhibitor antimycin-A, 2-deoxyglucose (2-DG), and GLUT1 inhibitor BAY876 were acquired from Sigma-Aldrich (St. Louis, MO).

    Techniques: Expressing, MANN-WHITNEY, Western Blot, Cell Culture, Software

    Effect of hypoxia or reagents on the cell surface expression of GLUT1. a HUVECs were cultured under normoxia or hypoxia as described in the Materials and Methods. In some experiments, the cells were treated with glibenclamide (Glb, 10 μM). The cells were labeled a human anti-GLUT1 Alexa Fluor 700-conjugated antibody to detect cell surface GLUT1. b Effect of CoCl 2 and/or glibenclamide on the cell surface expression of GLUT1. HUVECs were treated with CoCl 2 (100 µM) and/or glibenclamide (Glb, 10 μM). GLUT1 at the cell surface was determined as described in ( a ). ( a, b ) The histograms represent cell counts (Y-axis, linear scale) versus fluorescence intensity (X-axis, log scale). Fluorescence mean intensity obtained from the histograms was quantified and shown in bar graphs (right panels). Data are the mean ± SEM from 4 independent experiments. * P < 0.01 versus normoxia control (Mann–Whitney test). # P < 0.01 versus hypoxia without glibenclamide treatment (Mann–Whitney test)

    Journal: The Journal of Physiological Sciences : JPS

    Article Title: Hypoxia induces the translocation of glucose transporter 1 to the plasma membrane in vascular endothelial cells

    doi: 10.1186/s12576-020-00773-y

    Figure Lengend Snippet: Effect of hypoxia or reagents on the cell surface expression of GLUT1. a HUVECs were cultured under normoxia or hypoxia as described in the Materials and Methods. In some experiments, the cells were treated with glibenclamide (Glb, 10 μM). The cells were labeled a human anti-GLUT1 Alexa Fluor 700-conjugated antibody to detect cell surface GLUT1. b Effect of CoCl 2 and/or glibenclamide on the cell surface expression of GLUT1. HUVECs were treated with CoCl 2 (100 µM) and/or glibenclamide (Glb, 10 μM). GLUT1 at the cell surface was determined as described in ( a ). ( a, b ) The histograms represent cell counts (Y-axis, linear scale) versus fluorescence intensity (X-axis, log scale). Fluorescence mean intensity obtained from the histograms was quantified and shown in bar graphs (right panels). Data are the mean ± SEM from 4 independent experiments. * P < 0.01 versus normoxia control (Mann–Whitney test). # P < 0.01 versus hypoxia without glibenclamide treatment (Mann–Whitney test)

    Article Snippet: Anti-GLUT3 (PA5-72331) was obtained from Thermo Fisher (Waltham, MA). β-actin antibody (AC-74), ATP-sensitive potassium (KATP) channel inhibitor glibenclamide, mitochondrial KATP channel inhibitor 5-HD, ATP inhibitor antimycin-A, 2-deoxyglucose (2-DG), and GLUT1 inhibitor BAY876 were acquired from Sigma-Aldrich (St. Louis, MO).

    Techniques: Expressing, Cell Culture, Labeling, Fluorescence, MANN-WHITNEY

    GLUT1 expression on the cell surface. a HUVECs were cultured under normoxia or hypoxia as described in the Materials and Methods. In some experiments, the cells were treated with glibenclamide (Glb, 10 μM). a The cellular distribution of GLUT1 was determined by immunofluorescence staining. HUVECs were fixed with 4% paraformaldehyde and stained with an anti-GLUT1 antibody (green). Images were obtained with a confocal fluorescence microscope as described in the Materials and Methods. Representative images are shown from 4 independent experiments with similar results. Scale bars, 25 μm. b The number of cells in which GLUT1 was observed at the cell membrane was counted in approximately 100 cells from 4 or 5 independent experiments. Data are the mean ± SEM from 4 independent experiments. * P < 0.01 versus normoxia control (unpaired t -test). # P < 0.01 versus hypoxia without glibenclamide treatment (unpaired t -test)

    Journal: The Journal of Physiological Sciences : JPS

    Article Title: Hypoxia induces the translocation of glucose transporter 1 to the plasma membrane in vascular endothelial cells

    doi: 10.1186/s12576-020-00773-y

    Figure Lengend Snippet: GLUT1 expression on the cell surface. a HUVECs were cultured under normoxia or hypoxia as described in the Materials and Methods. In some experiments, the cells were treated with glibenclamide (Glb, 10 μM). a The cellular distribution of GLUT1 was determined by immunofluorescence staining. HUVECs were fixed with 4% paraformaldehyde and stained with an anti-GLUT1 antibody (green). Images were obtained with a confocal fluorescence microscope as described in the Materials and Methods. Representative images are shown from 4 independent experiments with similar results. Scale bars, 25 μm. b The number of cells in which GLUT1 was observed at the cell membrane was counted in approximately 100 cells from 4 or 5 independent experiments. Data are the mean ± SEM from 4 independent experiments. * P < 0.01 versus normoxia control (unpaired t -test). # P < 0.01 versus hypoxia without glibenclamide treatment (unpaired t -test)

    Article Snippet: Anti-GLUT3 (PA5-72331) was obtained from Thermo Fisher (Waltham, MA). β-actin antibody (AC-74), ATP-sensitive potassium (KATP) channel inhibitor glibenclamide, mitochondrial KATP channel inhibitor 5-HD, ATP inhibitor antimycin-A, 2-deoxyglucose (2-DG), and GLUT1 inhibitor BAY876 were acquired from Sigma-Aldrich (St. Louis, MO).

    Techniques: Expressing, Cell Culture, Immunofluorescence, Staining, Fluorescence, Microscopy

    Effect of hypoxia and reoxygenation on the cell-surface expression of GLUT1. a HUVECs were cultured under normoxia or 3 h or 12 h hypoxia, as described in the Materials and Methods. The cells were labeled with a human anti-GLUT1 Alexa Fluor ® 488-conjugated antibody to detect cell-surface GLUT1. b Effect of re-oxygenation on the cell-surface expression of GLUT1. HUVECs were cultured under 12 h hypoxia or 12 h normoxia following 12 h hypoxia. GLUT1 at the cell surface was determined as described in a . ( a, b ) The histograms represent cell counts (Y-axis, linear scale) versus fluorescence intensity (X-axis, log scale). Fluorescence mean intensity obtained from the histograms was quantified and shown in bar graphs (right panels). Data are the mean ± SEM from 4 independent experiments. * P < 0.01, # P < 0.05 vs. normoxia control (Mann–Whitney test). $ P < 0.01 vs. hypoxia (12 h) (Mann–Whitney test)

    Journal: The Journal of Physiological Sciences : JPS

    Article Title: Hypoxia induces the translocation of glucose transporter 1 to the plasma membrane in vascular endothelial cells

    doi: 10.1186/s12576-020-00773-y

    Figure Lengend Snippet: Effect of hypoxia and reoxygenation on the cell-surface expression of GLUT1. a HUVECs were cultured under normoxia or 3 h or 12 h hypoxia, as described in the Materials and Methods. The cells were labeled with a human anti-GLUT1 Alexa Fluor ® 488-conjugated antibody to detect cell-surface GLUT1. b Effect of re-oxygenation on the cell-surface expression of GLUT1. HUVECs were cultured under 12 h hypoxia or 12 h normoxia following 12 h hypoxia. GLUT1 at the cell surface was determined as described in a . ( a, b ) The histograms represent cell counts (Y-axis, linear scale) versus fluorescence intensity (X-axis, log scale). Fluorescence mean intensity obtained from the histograms was quantified and shown in bar graphs (right panels). Data are the mean ± SEM from 4 independent experiments. * P < 0.01, # P < 0.05 vs. normoxia control (Mann–Whitney test). $ P < 0.01 vs. hypoxia (12 h) (Mann–Whitney test)

    Article Snippet: Anti-GLUT3 (PA5-72331) was obtained from Thermo Fisher (Waltham, MA). β-actin antibody (AC-74), ATP-sensitive potassium (KATP) channel inhibitor glibenclamide, mitochondrial KATP channel inhibitor 5-HD, ATP inhibitor antimycin-A, 2-deoxyglucose (2-DG), and GLUT1 inhibitor BAY876 were acquired from Sigma-Aldrich (St. Louis, MO).

    Techniques: Expressing, Cell Culture, Labeling, Fluorescence, MANN-WHITNEY

    ATP concentration and GLUT1 expression in HUVECs. a Intracellular ATP production was measured following culture of the cells under normoxia or hypoxia, with or without glibenclamide (Glb, 10 μM), as described in the Materials and Methods. Data are expressed as the mean ± SEM from 4 independent experiments. * P < 0.01 vs. normoxic control without glibenclamide treatment (Mann–Whitney test). b HUVECs in 96-well plates were treated with antimycin-A (Anti-A, 10 μM) or 2-deoxyglucose (2-DG, 1 mM) for 30 min at normoxia. In some groups, the cells were also treated with glibenclamide (Glb, 10 μM). ATP was measured as described in the Materials and Methods. Data are from experiments performed in duplicate. * P < 0.01 compared with control without glibenclamide treatment (Mann–Whitney test). c HUVECs were treated with CoCl 2 (100 μM) with or without glibenclamide (Glb, 10 μM). Intracellular ATP concentration was analyzed as described in the “ ”. Data are expressed as the mean ± SEM from 4 independent experiments. No statistical significance was detected by the Mann–Whitney test. d GLUT1 expression determined by immunoblotting following treatment with antimycin-A (Anti-A, 10 μM), 2-deoxyglucose (2-DG, 1 mM), CoCl 2 (100 µM), and/or glibenclamide (Glb, 10 μM). Data are expressed as the mean ± SEM from 4 independent experiments. # P < 0.05 versus vehicle control without glibenclamide treatment (Mann–Whitney test)

    Journal: The Journal of Physiological Sciences : JPS

    Article Title: Hypoxia induces the translocation of glucose transporter 1 to the plasma membrane in vascular endothelial cells

    doi: 10.1186/s12576-020-00773-y

    Figure Lengend Snippet: ATP concentration and GLUT1 expression in HUVECs. a Intracellular ATP production was measured following culture of the cells under normoxia or hypoxia, with or without glibenclamide (Glb, 10 μM), as described in the Materials and Methods. Data are expressed as the mean ± SEM from 4 independent experiments. * P < 0.01 vs. normoxic control without glibenclamide treatment (Mann–Whitney test). b HUVECs in 96-well plates were treated with antimycin-A (Anti-A, 10 μM) or 2-deoxyglucose (2-DG, 1 mM) for 30 min at normoxia. In some groups, the cells were also treated with glibenclamide (Glb, 10 μM). ATP was measured as described in the Materials and Methods. Data are from experiments performed in duplicate. * P < 0.01 compared with control without glibenclamide treatment (Mann–Whitney test). c HUVECs were treated with CoCl 2 (100 μM) with or without glibenclamide (Glb, 10 μM). Intracellular ATP concentration was analyzed as described in the “ ”. Data are expressed as the mean ± SEM from 4 independent experiments. No statistical significance was detected by the Mann–Whitney test. d GLUT1 expression determined by immunoblotting following treatment with antimycin-A (Anti-A, 10 μM), 2-deoxyglucose (2-DG, 1 mM), CoCl 2 (100 µM), and/or glibenclamide (Glb, 10 μM). Data are expressed as the mean ± SEM from 4 independent experiments. # P < 0.05 versus vehicle control without glibenclamide treatment (Mann–Whitney test)

    Article Snippet: Anti-GLUT3 (PA5-72331) was obtained from Thermo Fisher (Waltham, MA). β-actin antibody (AC-74), ATP-sensitive potassium (KATP) channel inhibitor glibenclamide, mitochondrial KATP channel inhibitor 5-HD, ATP inhibitor antimycin-A, 2-deoxyglucose (2-DG), and GLUT1 inhibitor BAY876 were acquired from Sigma-Aldrich (St. Louis, MO).

    Techniques: Concentration Assay, Expressing, MANN-WHITNEY, Western Blot

    Effects of reagents decreasing cellular ATP levels on the cell surface expression of GLUT1. HUVECs were treated with antimycin-A (Anti-A, 10 μM) ( a ) or 2-deoxyglucose (2-DG, 1 mM) ( b ) for 30 min at normoxia. In some groups, the cells were also treated with glibenclamide (Glb, 10 μM). The cells were labeled with a human anti-GLUT1 Alexa Fluor 700-conjugated antibody to detect GLUT1 on the cell surface. ( a, b ) The histograms represent cell counts (Y-axis, linear scale) versus fluorescence intensity (X-axis, log scale). Fluorescence mean intensity obtained from the histograms was quantified and shown in bar graphs (right panels). Data are the mean ± SEM from 4 independent experiments. * P < 0.01 versus normoxia control (Mann–Whitney test). # P < 0.01 versus antimycin-A (Mann–Whitney test). $ P < 0.01 versus 2-deoxyglucose (Mann–Whitney test)

    Journal: The Journal of Physiological Sciences : JPS

    Article Title: Hypoxia induces the translocation of glucose transporter 1 to the plasma membrane in vascular endothelial cells

    doi: 10.1186/s12576-020-00773-y

    Figure Lengend Snippet: Effects of reagents decreasing cellular ATP levels on the cell surface expression of GLUT1. HUVECs were treated with antimycin-A (Anti-A, 10 μM) ( a ) or 2-deoxyglucose (2-DG, 1 mM) ( b ) for 30 min at normoxia. In some groups, the cells were also treated with glibenclamide (Glb, 10 μM). The cells were labeled with a human anti-GLUT1 Alexa Fluor 700-conjugated antibody to detect GLUT1 on the cell surface. ( a, b ) The histograms represent cell counts (Y-axis, linear scale) versus fluorescence intensity (X-axis, log scale). Fluorescence mean intensity obtained from the histograms was quantified and shown in bar graphs (right panels). Data are the mean ± SEM from 4 independent experiments. * P < 0.01 versus normoxia control (Mann–Whitney test). # P < 0.01 versus antimycin-A (Mann–Whitney test). $ P < 0.01 versus 2-deoxyglucose (Mann–Whitney test)

    Article Snippet: Anti-GLUT3 (PA5-72331) was obtained from Thermo Fisher (Waltham, MA). β-actin antibody (AC-74), ATP-sensitive potassium (KATP) channel inhibitor glibenclamide, mitochondrial KATP channel inhibitor 5-HD, ATP inhibitor antimycin-A, 2-deoxyglucose (2-DG), and GLUT1 inhibitor BAY876 were acquired from Sigma-Aldrich (St. Louis, MO).

    Techniques: Expressing, Labeling, Fluorescence, MANN-WHITNEY

    Effects of reagents decreasing cellular ATP levels on the subcellular localization of GLUT1. a HUVECs were treated with antimycin-A (Anti-A, 10 μM) or 2-deoxyglucose (2-DG, 1 mM) with or without glibenclamide (Glb, 10 μM) under normoxia. The cellular distribution of GLUT1 was determined by immunofluorescence staining as described in the Materials and Methods. HUVECs were stained with an anti-GLUT1 antibody (green). Images were obtained with a confocal fluorescence microscope as described in the “ ”. Representative images are shown from 4 independent experiments with similar results. Scale bars, 25 μm. b The number of cells in which GLUT1 was observed at the cell membrane was counted in approximately 100 cells from 4 or 5 independent experiments. Data are the mean ± SEM from 4 independent experiments. * P < 0.01 versus normoxia control without glibenclamide treatment (unpaired t -test). # P < 0.01 versus antimycin-A without glibenclamide treatment (unpaired t -test). $ P < 0.01 versus 2-deoxyglucose without glibenclamide treatment (unpaired t -test)

    Journal: The Journal of Physiological Sciences : JPS

    Article Title: Hypoxia induces the translocation of glucose transporter 1 to the plasma membrane in vascular endothelial cells

    doi: 10.1186/s12576-020-00773-y

    Figure Lengend Snippet: Effects of reagents decreasing cellular ATP levels on the subcellular localization of GLUT1. a HUVECs were treated with antimycin-A (Anti-A, 10 μM) or 2-deoxyglucose (2-DG, 1 mM) with or without glibenclamide (Glb, 10 μM) under normoxia. The cellular distribution of GLUT1 was determined by immunofluorescence staining as described in the Materials and Methods. HUVECs were stained with an anti-GLUT1 antibody (green). Images were obtained with a confocal fluorescence microscope as described in the “ ”. Representative images are shown from 4 independent experiments with similar results. Scale bars, 25 μm. b The number of cells in which GLUT1 was observed at the cell membrane was counted in approximately 100 cells from 4 or 5 independent experiments. Data are the mean ± SEM from 4 independent experiments. * P < 0.01 versus normoxia control without glibenclamide treatment (unpaired t -test). # P < 0.01 versus antimycin-A without glibenclamide treatment (unpaired t -test). $ P < 0.01 versus 2-deoxyglucose without glibenclamide treatment (unpaired t -test)

    Article Snippet: Anti-GLUT3 (PA5-72331) was obtained from Thermo Fisher (Waltham, MA). β-actin antibody (AC-74), ATP-sensitive potassium (KATP) channel inhibitor glibenclamide, mitochondrial KATP channel inhibitor 5-HD, ATP inhibitor antimycin-A, 2-deoxyglucose (2-DG), and GLUT1 inhibitor BAY876 were acquired from Sigma-Aldrich (St. Louis, MO).

    Techniques: Immunofluorescence, Staining, Fluorescence, Microscopy

    Effects of the mitochondrial KATP channel inhibitor 5-HD on the cell surface expression of GLUT1. HUVECs were cultured under normoxia or hypoxia with or without 5-HD (100 μM). a Cell surface expression of GLUT1 determined by flow cytometric analysis. The cells were labeled with a human anti-GLUT1 Alexa Fluor 700-conjugated antibody to detect cell surface GLUT1. Left panel: The histograms represent cell counts (Y-axis, linear scale) versus fluorescence intensity (X-axis, log scale). Right panel: Fluorescence mean intensity obtained from the histograms was quantified and shown in bar graphs (right panels). Data are the mean ± SEM from 4 independent experiments. * P < 0.01 versus normoxia control (Mann–Whitney test). b The cellular distribution of GLUT1 was determined by immunofluorescence staining as described in the Materials and Methods. HUVECs were stained with an anti-GLUT1 antibody (green). Left panel: Images were obtained with a confocal fluorescence microscope as described in the “ ”. Representative images are shown from 4 independent experiments with similar results. Scale bars, 25 μm. Right panel: The number of cells in which GLUT1 was observed at the cell membrane was counted in approximately 100 cells from 4 independent experiments. Data are the mean ± SEM from 4 independent experiments. * P < 0.01 versus normoxia control (Mann–Whitney test)

    Journal: The Journal of Physiological Sciences : JPS

    Article Title: Hypoxia induces the translocation of glucose transporter 1 to the plasma membrane in vascular endothelial cells

    doi: 10.1186/s12576-020-00773-y

    Figure Lengend Snippet: Effects of the mitochondrial KATP channel inhibitor 5-HD on the cell surface expression of GLUT1. HUVECs were cultured under normoxia or hypoxia with or without 5-HD (100 μM). a Cell surface expression of GLUT1 determined by flow cytometric analysis. The cells were labeled with a human anti-GLUT1 Alexa Fluor 700-conjugated antibody to detect cell surface GLUT1. Left panel: The histograms represent cell counts (Y-axis, linear scale) versus fluorescence intensity (X-axis, log scale). Right panel: Fluorescence mean intensity obtained from the histograms was quantified and shown in bar graphs (right panels). Data are the mean ± SEM from 4 independent experiments. * P < 0.01 versus normoxia control (Mann–Whitney test). b The cellular distribution of GLUT1 was determined by immunofluorescence staining as described in the Materials and Methods. HUVECs were stained with an anti-GLUT1 antibody (green). Left panel: Images were obtained with a confocal fluorescence microscope as described in the “ ”. Representative images are shown from 4 independent experiments with similar results. Scale bars, 25 μm. Right panel: The number of cells in which GLUT1 was observed at the cell membrane was counted in approximately 100 cells from 4 independent experiments. Data are the mean ± SEM from 4 independent experiments. * P < 0.01 versus normoxia control (Mann–Whitney test)

    Article Snippet: Anti-GLUT3 (PA5-72331) was obtained from Thermo Fisher (Waltham, MA). β-actin antibody (AC-74), ATP-sensitive potassium (KATP) channel inhibitor glibenclamide, mitochondrial KATP channel inhibitor 5-HD, ATP inhibitor antimycin-A, 2-deoxyglucose (2-DG), and GLUT1 inhibitor BAY876 were acquired from Sigma-Aldrich (St. Louis, MO).

    Techniques: Expressing, Cell Culture, Labeling, Fluorescence, MANN-WHITNEY, Immunofluorescence, Staining, Microscopy

    Expression of  GLUT1,  GLUT3, and KATP channel subunits in HUVECs under normoxia and hypoxia

    Journal: The Journal of Physiological Sciences : JPS

    Article Title: Hypoxia induces the translocation of glucose transporter 1 to the plasma membrane in vascular endothelial cells

    doi: 10.1186/s12576-020-00773-y

    Figure Lengend Snippet: Expression of GLUT1, GLUT3, and KATP channel subunits in HUVECs under normoxia and hypoxia

    Article Snippet: Anti-GLUT3 (PA5-72331) was obtained from Thermo Fisher (Waltham, MA). β-actin antibody (AC-74), ATP-sensitive potassium (KATP) channel inhibitor glibenclamide, mitochondrial KATP channel inhibitor 5-HD, ATP inhibitor antimycin-A, 2-deoxyglucose (2-DG), and GLUT1 inhibitor BAY876 were acquired from Sigma-Aldrich (St. Louis, MO).

    Techniques: Expressing