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  • 98
    Millipore 6 aminonicotinamide 6 an
    6 Aminonicotinamide 6 An, supplied by Millipore, used in various techniques. Bioz Stars score: 98/100, based on 34 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/6 aminonicotinamide 6 an/product/Millipore
    Average 98 stars, based on 34 article reviews
    Price from $9.99 to $1999.99
    6 aminonicotinamide 6 an - by Bioz Stars, 2020-10
    98/100 stars
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    94
    Cayman Chemical 6 aminonicotinamide
    T-antigen is downregulated by glucose deprivation through specific glycolytic pathways and influences the glycolytic enzyme expression profile of medulloblastoma cells. BsB8 cells were treated with the indicated doses of 2-deoxy-D-glucose (2-DG) (A), oxamate (B), <t>6-aminonicotinamide</t> (6-AN) (C), and oxythiamine (D) for 24 hours, and T-antigen expression was measured by western blot. E. Bs1a, Bs1f, and BsB8 cells were exposed to glucose deprivation for 24 hours, and glycolytic enzyme expression was measured by western blot. F. HJC-2 cells were transduced with lentivirus expressing Large T-antigen, scrambled shRNA, or were non-transduced and then exposed to glucose deprivation for 16 hours. Glycolytic enzyme expression was measured by western blot. G. Quantification of HEK2 expression relative to Grb2 in F. C, control; GD, glucose deprivation.
    6 Aminonicotinamide, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 94/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/6 aminonicotinamide/product/Cayman Chemical
    Average 94 stars, based on 13 article reviews
    Price from $9.99 to $1999.99
    6 aminonicotinamide - by Bioz Stars, 2020-10
    94/100 stars
      Buy from Supplier

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    T-antigen is downregulated by glucose deprivation through specific glycolytic pathways and influences the glycolytic enzyme expression profile of medulloblastoma cells. BsB8 cells were treated with the indicated doses of 2-deoxy-D-glucose (2-DG) (A), oxamate (B), 6-aminonicotinamide (6-AN) (C), and oxythiamine (D) for 24 hours, and T-antigen expression was measured by western blot. E. Bs1a, Bs1f, and BsB8 cells were exposed to glucose deprivation for 24 hours, and glycolytic enzyme expression was measured by western blot. F. HJC-2 cells were transduced with lentivirus expressing Large T-antigen, scrambled shRNA, or were non-transduced and then exposed to glucose deprivation for 16 hours. Glycolytic enzyme expression was measured by western blot. G. Quantification of HEK2 expression relative to Grb2 in F. C, control; GD, glucose deprivation.

    Journal: PLoS ONE

    Article Title: JC Virus T-Antigen Regulates Glucose Metabolic Pathways in Brain Tumor Cells

    doi: 10.1371/journal.pone.0035054

    Figure Lengend Snippet: T-antigen is downregulated by glucose deprivation through specific glycolytic pathways and influences the glycolytic enzyme expression profile of medulloblastoma cells. BsB8 cells were treated with the indicated doses of 2-deoxy-D-glucose (2-DG) (A), oxamate (B), 6-aminonicotinamide (6-AN) (C), and oxythiamine (D) for 24 hours, and T-antigen expression was measured by western blot. E. Bs1a, Bs1f, and BsB8 cells were exposed to glucose deprivation for 24 hours, and glycolytic enzyme expression was measured by western blot. F. HJC-2 cells were transduced with lentivirus expressing Large T-antigen, scrambled shRNA, or were non-transduced and then exposed to glucose deprivation for 16 hours. Glycolytic enzyme expression was measured by western blot. G. Quantification of HEK2 expression relative to Grb2 in F. C, control; GD, glucose deprivation.

    Article Snippet: Treatment of BsB8 cells with 6-aminonicotinamide (6-AN), an inhibitor of glucose 6-phosphate dehydrogenase (G6PDH), the rate-limiting enzyme in the pentose phosphate pathway, resulted in marked downregulation of T-antigen in a dose-dependent manner ( ).

    Techniques: Expressing, Western Blot, Transduction, shRNA

    Mechanism and significance of metabolic signaling pathways affected by the presence of JCV T-antigen. JCV T-antigen is downregulated by glucose deprivation in an AMPK-dependent manner. During periods of glucose deprivation, T-antigen inhibits AMPK phosphorylation, which prevents the induction of reactive oxygen species (ROS) and subsequent cytotoxicity. Additionally, T-antigen relieves AMPK-mediated cyclin B1 and cyclin A inhibition, leading to decreased G1 arrest. Glucose deprivation induces both enhanced glycolytic flux to maintain high levels of ATP production as well as enhanced pentose phosphate pathway activation to supply reducing equivalents in the form of reduced nicotinamide adenine dinucleotide phosphate (NADPH) to counteract ROS production produced by glycolysis. T-antigen upregulates transaldolase-1 (TALDO1) expression to shift intermediates from the pentose phosphate pathway towards glycolysis to enhance ATP production and also prevents hexokinase 2 (HK2) upregulation during glucose deprivation. (HK2, hexokinase; G6PDH, glucose 6-phosphate dehydrogenase; 6-PGDH, 6-phoshogluconate dehydrogenase; TKTL, transketolase; PKM2, pyruvate kinase M2; LDH, lactate dehydrogenase; 2-DG, 2-deoxyglucose; 6-AN, 6-aminonicotinamide; OT, oxythiamine).

    Journal: PLoS ONE

    Article Title: JC Virus T-Antigen Regulates Glucose Metabolic Pathways in Brain Tumor Cells

    doi: 10.1371/journal.pone.0035054

    Figure Lengend Snippet: Mechanism and significance of metabolic signaling pathways affected by the presence of JCV T-antigen. JCV T-antigen is downregulated by glucose deprivation in an AMPK-dependent manner. During periods of glucose deprivation, T-antigen inhibits AMPK phosphorylation, which prevents the induction of reactive oxygen species (ROS) and subsequent cytotoxicity. Additionally, T-antigen relieves AMPK-mediated cyclin B1 and cyclin A inhibition, leading to decreased G1 arrest. Glucose deprivation induces both enhanced glycolytic flux to maintain high levels of ATP production as well as enhanced pentose phosphate pathway activation to supply reducing equivalents in the form of reduced nicotinamide adenine dinucleotide phosphate (NADPH) to counteract ROS production produced by glycolysis. T-antigen upregulates transaldolase-1 (TALDO1) expression to shift intermediates from the pentose phosphate pathway towards glycolysis to enhance ATP production and also prevents hexokinase 2 (HK2) upregulation during glucose deprivation. (HK2, hexokinase; G6PDH, glucose 6-phosphate dehydrogenase; 6-PGDH, 6-phoshogluconate dehydrogenase; TKTL, transketolase; PKM2, pyruvate kinase M2; LDH, lactate dehydrogenase; 2-DG, 2-deoxyglucose; 6-AN, 6-aminonicotinamide; OT, oxythiamine).

    Article Snippet: Treatment of BsB8 cells with 6-aminonicotinamide (6-AN), an inhibitor of glucose 6-phosphate dehydrogenase (G6PDH), the rate-limiting enzyme in the pentose phosphate pathway, resulted in marked downregulation of T-antigen in a dose-dependent manner ( ).

    Techniques: Inhibition, Activation Assay, Produced, Expressing