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Inhibition of p53 promotes metabolic alterations in the kidney consistent with an increased glycolytic flux. A: representative confocal images of TP53-induced glycolysis and <t>apoptosis</t> regulator (TIGAR) immunofluorescent staining (blue) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of TIGAR immunostaining. B: representative confocal images of pyruvate dehydrogenase kinase 1 (PDK1) immunofluorescent staining (yellow) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of PDK1 immunostaining. C: pyruvate dehydrogenase (PDH) activity in kidney homogenate obtained from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Each tracing represents an individual animal, P < 0.001. D: data plots of key glycolytic metabolites as determined by a nonbiased metabolomics screen using ultra-high performance liquid chromatography-tandem mass spectroscopy. Each data point represents the measured metabolite from an individual animal in the associated treatment group as a scaled intensity compared with an internal standard.
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Inhibition of p53 promotes metabolic alterations in the kidney consistent with an increased glycolytic flux. A: representative confocal images of TP53-induced glycolysis and <t>apoptosis</t> regulator (TIGAR) immunofluorescent staining (blue) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of TIGAR immunostaining. B: representative confocal images of pyruvate dehydrogenase kinase 1 (PDK1) immunofluorescent staining (yellow) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of PDK1 immunostaining. C: pyruvate dehydrogenase (PDH) activity in kidney homogenate obtained from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Each tracing represents an individual animal, P < 0.001. D: data plots of key glycolytic metabolites as determined by a nonbiased metabolomics screen using ultra-high performance liquid chromatography-tandem mass spectroscopy. Each data point represents the measured metabolite from an individual animal in the associated treatment group as a scaled intensity compared with an internal standard.
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Inhibition of p53 promotes metabolic alterations in the kidney consistent with an increased glycolytic flux. A: representative confocal images of TP53-induced glycolysis and <t>apoptosis</t> regulator (TIGAR) immunofluorescent staining (blue) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of TIGAR immunostaining. B: representative confocal images of pyruvate dehydrogenase kinase 1 (PDK1) immunofluorescent staining (yellow) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of PDK1 immunostaining. C: pyruvate dehydrogenase (PDH) activity in kidney homogenate obtained from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Each tracing represents an individual animal, P < 0.001. D: data plots of key glycolytic metabolites as determined by a nonbiased metabolomics screen using ultra-high performance liquid chromatography-tandem mass spectroscopy. Each data point represents the measured metabolite from an individual animal in the associated treatment group as a scaled intensity compared with an internal standard.
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Inhibition of p53 promotes metabolic alterations in the kidney consistent with an increased glycolytic flux. A: representative confocal images of TP53-induced glycolysis and <t>apoptosis</t> regulator (TIGAR) immunofluorescent staining (blue) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of TIGAR immunostaining. B: representative confocal images of pyruvate dehydrogenase kinase 1 (PDK1) immunofluorescent staining (yellow) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of PDK1 immunostaining. C: pyruvate dehydrogenase (PDH) activity in kidney homogenate obtained from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Each tracing represents an individual animal, P < 0.001. D: data plots of key glycolytic metabolites as determined by a nonbiased metabolomics screen using ultra-high performance liquid chromatography-tandem mass spectroscopy. Each data point represents the measured metabolite from an individual animal in the associated treatment group as a scaled intensity compared with an internal standard.
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Inhibition of p53 promotes metabolic alterations in the kidney consistent with an increased glycolytic flux. A: representative confocal images of TP53-induced glycolysis and <t>apoptosis</t> regulator (TIGAR) immunofluorescent staining (blue) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of TIGAR immunostaining. B: representative confocal images of pyruvate dehydrogenase kinase 1 (PDK1) immunofluorescent staining (yellow) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of PDK1 immunostaining. C: pyruvate dehydrogenase (PDH) activity in kidney homogenate obtained from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Each tracing represents an individual animal, P < 0.001. D: data plots of key glycolytic metabolites as determined by a nonbiased metabolomics screen using ultra-high performance liquid chromatography-tandem mass spectroscopy. Each data point represents the measured metabolite from an individual animal in the associated treatment group as a scaled intensity compared with an internal standard.
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Inhibition of p53 promotes metabolic alterations in the kidney consistent with an increased glycolytic flux. A: representative confocal images of TP53-induced glycolysis and <t>apoptosis</t> regulator (TIGAR) immunofluorescent staining (blue) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of TIGAR immunostaining. B: representative confocal images of pyruvate dehydrogenase kinase 1 (PDK1) immunofluorescent staining (yellow) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of PDK1 immunostaining. C: pyruvate dehydrogenase (PDH) activity in kidney homogenate obtained from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Each tracing represents an individual animal, P < 0.001. D: data plots of key glycolytic metabolites as determined by a nonbiased metabolomics screen using ultra-high performance liquid chromatography-tandem mass spectroscopy. Each data point represents the measured metabolite from an individual animal in the associated treatment group as a scaled intensity compared with an internal standard.
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Inhibition of p53 promotes metabolic alterations in the kidney consistent with an increased glycolytic flux. A: representative confocal images of TP53-induced glycolysis and <t>apoptosis</t> regulator (TIGAR) immunofluorescent staining (blue) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of TIGAR immunostaining. B: representative confocal images of pyruvate dehydrogenase kinase 1 (PDK1) immunofluorescent staining (yellow) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of PDK1 immunostaining. C: pyruvate dehydrogenase (PDH) activity in kidney homogenate obtained from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Each tracing represents an individual animal, P < 0.001. D: data plots of key glycolytic metabolites as determined by a nonbiased metabolomics screen using ultra-high performance liquid chromatography-tandem mass spectroscopy. Each data point represents the measured metabolite from an individual animal in the associated treatment group as a scaled intensity compared with an internal standard.
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Inhibition of p53 promotes metabolic alterations in the kidney consistent with an increased glycolytic flux. A: representative confocal images of TP53-induced glycolysis and <t>apoptosis</t> regulator (TIGAR) immunofluorescent staining (blue) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of TIGAR immunostaining. B: representative confocal images of pyruvate dehydrogenase kinase 1 (PDK1) immunofluorescent staining (yellow) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of PDK1 immunostaining. C: pyruvate dehydrogenase (PDH) activity in kidney homogenate obtained from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Each tracing represents an individual animal, P < 0.001. D: data plots of key glycolytic metabolites as determined by a nonbiased metabolomics screen using ultra-high performance liquid chromatography-tandem mass spectroscopy. Each data point represents the measured metabolite from an individual animal in the associated treatment group as a scaled intensity compared with an internal standard.
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Inhibition of p53 promotes metabolic alterations in the kidney consistent with an increased glycolytic flux. A: representative confocal images of TP53-induced glycolysis and <t>apoptosis</t> regulator (TIGAR) immunofluorescent staining (blue) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of TIGAR immunostaining. B: representative confocal images of pyruvate dehydrogenase kinase 1 (PDK1) immunofluorescent staining (yellow) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of PDK1 immunostaining. C: pyruvate dehydrogenase (PDH) activity in kidney homogenate obtained from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Each tracing represents an individual animal, P < 0.001. D: data plots of key glycolytic metabolites as determined by a nonbiased metabolomics screen using ultra-high performance liquid chromatography-tandem mass spectroscopy. Each data point represents the measured metabolite from an individual animal in the associated treatment group as a scaled intensity compared with an internal standard.
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Inhibition of p53 promotes metabolic alterations in the kidney consistent with an increased glycolytic flux. A: representative confocal images of TP53-induced glycolysis and <t>apoptosis</t> regulator (TIGAR) immunofluorescent staining (blue) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of TIGAR immunostaining. B: representative confocal images of pyruvate dehydrogenase kinase 1 (PDK1) immunofluorescent staining (yellow) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of PDK1 immunostaining. C: pyruvate dehydrogenase (PDH) activity in kidney homogenate obtained from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Each tracing represents an individual animal, P < 0.001. D: data plots of key glycolytic metabolites as determined by a nonbiased metabolomics screen using ultra-high performance liquid chromatography-tandem mass spectroscopy. Each data point represents the measured metabolite from an individual animal in the associated treatment group as a scaled intensity compared with an internal standard.
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Inhibition of p53 promotes metabolic alterations in the kidney consistent with an increased glycolytic flux. A: representative confocal images of TP53-induced glycolysis and <t>apoptosis</t> regulator (TIGAR) immunofluorescent staining (blue) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of TIGAR immunostaining. B: representative confocal images of pyruvate dehydrogenase kinase 1 (PDK1) immunofluorescent staining (yellow) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of PDK1 immunostaining. C: pyruvate dehydrogenase (PDH) activity in kidney homogenate obtained from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Each tracing represents an individual animal, P < 0.001. D: data plots of key glycolytic metabolites as determined by a nonbiased metabolomics screen using ultra-high performance liquid chromatography-tandem mass spectroscopy. Each data point represents the measured metabolite from an individual animal in the associated treatment group as a scaled intensity compared with an internal standard.
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Image Search Results


Inhibition of p53 promotes metabolic alterations in the kidney consistent with an increased glycolytic flux. A: representative confocal images of TP53-induced glycolysis and apoptosis regulator (TIGAR) immunofluorescent staining (blue) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of TIGAR immunostaining. B: representative confocal images of pyruvate dehydrogenase kinase 1 (PDK1) immunofluorescent staining (yellow) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of PDK1 immunostaining. C: pyruvate dehydrogenase (PDH) activity in kidney homogenate obtained from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Each tracing represents an individual animal, P < 0.001. D: data plots of key glycolytic metabolites as determined by a nonbiased metabolomics screen using ultra-high performance liquid chromatography-tandem mass spectroscopy. Each data point represents the measured metabolite from an individual animal in the associated treatment group as a scaled intensity compared with an internal standard.

Journal: American Journal of Physiology - Renal Physiology

Article Title: Novel application of complementary imaging techniques to examine in vivo glucose metabolism in the kidney

doi: 10.1152/ajprenal.00535.2015

Figure Lengend Snippet: Inhibition of p53 promotes metabolic alterations in the kidney consistent with an increased glycolytic flux. A: representative confocal images of TP53-induced glycolysis and apoptosis regulator (TIGAR) immunofluorescent staining (blue) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of TIGAR immunostaining. B: representative confocal images of pyruvate dehydrogenase kinase 1 (PDK1) immunofluorescent staining (yellow) in the cortex of kidneys from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Right: quantitation of PDK1 immunostaining. C: pyruvate dehydrogenase (PDH) activity in kidney homogenate obtained from sham animals (vehicle control = DMSO) and animals treated with pifithrin-α. Each tracing represents an individual animal, P < 0.001. D: data plots of key glycolytic metabolites as determined by a nonbiased metabolomics screen using ultra-high performance liquid chromatography-tandem mass spectroscopy. Each data point represents the measured metabolite from an individual animal in the associated treatment group as a scaled intensity compared with an internal standard.

Article Snippet: The following primary antibodies were used for immunostaining: TP53-induced glycolysis and apoptosis regulator (TIGAR; IN1) rabbit polyclonal (ProSci) and pyruvate dehydrogenase kinase 1 (PDK1) rabbit polyclonal (Enzo Life Sciences).

Techniques: Inhibition, Staining, Quantitation Assay, Immunostaining, Activity Assay, High Performance Liquid Chromatography, Tandem Mass Spectroscopy