6 aminonicotinamide  (Cayman Chemical)

 
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    Name:
    6 Aminonicotinamide
    Description:
    6 Aminonicotinamide 6 AN is a well established inhibitor of the NADP dependent enzyme 6 phosphogluconate dehydrogenase K 0 46 μM Through this action 6 AN interferes with glycolysis resulting in ATP depletion and synergizes with DNA crosslinking chemotherapy drugs like cisplatin in killing cancer cells IC 0 5 mM 6 AN also reduces cardiovascular oxidative injury following ischemia reperfusion In addition 6 AN causes glial neurodegeneration
    Catalog Number:
    10009315
    Product Aliases:
    6-,AN,NSC 21206,SR 4388
    Price:
    $10
    Purity:
    ≥98%
    Size:
    100 mg
    Formula:
    A crystalline solid
    Buy from Supplier


    Structured Review

    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 6 AN is a well established inhibitor of the NADP dependent enzyme 6 phosphogluconate dehydrogenase K 0 46 μM Through this action 6 AN interferes with glycolysis resulting in ATP depletion and synergizes with DNA crosslinking chemotherapy drugs like cisplatin in killing cancer cells IC 0 5 mM 6 AN also reduces cardiovascular oxidative injury following ischemia reperfusion In addition 6 AN causes glial neurodegeneration
    https://www.bioz.com/result/6 aminonicotinamide/product/Cayman Chemical
    Average 94 stars, based on 4 article reviews
    Price from $9.99 to $1999.99
    6 aminonicotinamide - by Bioz Stars, 2020-11
    94/100 stars

    Images

    1) Product Images from "JC Virus T-Antigen Regulates Glucose Metabolic Pathways in Brain Tumor Cells"

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

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0035054

    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.
    Figure Legend 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.

    Techniques Used: 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).
    Figure Legend 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).

    Techniques Used: Inhibition, Activation Assay, Produced, Expressing

    2) Product Images from "JC Virus T-Antigen Regulates Glucose Metabolic Pathways in Brain Tumor Cells"

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

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0035054

    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.
    Figure Legend 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.

    Techniques Used: 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).
    Figure Legend 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).

    Techniques Used: Inhibition, Activation Assay, Produced, Expressing

    Related Articles

    MTS Assay:

    Article Title: Distinct initiating events underpin the immune and metabolic heterogeneity of KRAS-mutant lung adenocarcinoma
    Article Snippet: .. 6-AN treatment study For in vitro single dose studies, A549, H460, H358 and H441 cell lines were treated with 62.5 μM 6-AN (Cayman Chemicals #10009315) for 72 h, and cell survival was then measured using the MTS assay (CellTiter96 Aqueous Non-Radioactive Cell Proliferation Assay, Promega) relative to DMSO vehicle treated cells. ..

    other:

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

    Article Title: Novel diagnostics of metabolic dysfunction detected in breath and plasma by selective isotope assisted labeling (SIAL)
    Article Snippet: 6-Aminonicotinamide (6-AN) was from Cayman Chemical Company, Ann Arbor, MI, USA.

    Proliferation Assay:

    Article Title: Distinct initiating events underpin the immune and metabolic heterogeneity of KRAS-mutant lung adenocarcinoma
    Article Snippet: .. 6-AN treatment study For in vitro single dose studies, A549, H460, H358 and H441 cell lines were treated with 62.5 μM 6-AN (Cayman Chemicals #10009315) for 72 h, and cell survival was then measured using the MTS assay (CellTiter96 Aqueous Non-Radioactive Cell Proliferation Assay, Promega) relative to DMSO vehicle treated cells. ..

    In Vitro:

    Article Title: Distinct initiating events underpin the immune and metabolic heterogeneity of KRAS-mutant lung adenocarcinoma
    Article Snippet: .. 6-AN treatment study For in vitro single dose studies, A549, H460, H358 and H441 cell lines were treated with 62.5 μM 6-AN (Cayman Chemicals #10009315) for 72 h, and cell survival was then measured using the MTS assay (CellTiter96 Aqueous Non-Radioactive Cell Proliferation Assay, Promega) relative to DMSO vehicle treated cells. ..

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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 6 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 6 article reviews
    Price from $9.99 to $1999.99
    6 aminonicotinamide - by Bioz Stars, 2020-11
    94/100 stars
      Buy from Supplier

    Image Search Results


    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: Fenofibrate (Sigma), 2-deoxy-D-glucose (Sigma), sodium oxamate (Sigma), 6-aminonicotinamide (Cayman Chemical), and oxythiamine (MP Biomedicals) were used at the indicated doses.

    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: Fenofibrate (Sigma), 2-deoxy-D-glucose (Sigma), sodium oxamate (Sigma), 6-aminonicotinamide (Cayman Chemical), and oxythiamine (MP Biomedicals) were used at the indicated doses.

    Techniques: Inhibition, Activation Assay, Produced, Expressing

    Increased oxidative stress was induced by 10 mM 6AN or 0.1 mM PQ. The oxidative marker GSSG were increased at 24 h post blood meal. ( a ) Protein carbonylation and GSSG/GSH ratios. Each symbol represents data from a pool of 30 females; the central line denotes the mean with a standard error bar. Statistically significant comparisons are denoted with an asterisk. GSSG/GSH ratio in 10 mM 6AN was significantly increased (One-Way ANOVA, P

    Journal: Scientific Reports

    Article Title: Redox state affects fecundity and insecticide susceptibility in Anopheles gambiae

    doi: 10.1038/s41598-018-31360-2

    Figure Lengend Snippet: Increased oxidative stress was induced by 10 mM 6AN or 0.1 mM PQ. The oxidative marker GSSG were increased at 24 h post blood meal. ( a ) Protein carbonylation and GSSG/GSH ratios. Each symbol represents data from a pool of 30 females; the central line denotes the mean with a standard error bar. Statistically significant comparisons are denoted with an asterisk. GSSG/GSH ratio in 10 mM 6AN was significantly increased (One-Way ANOVA, P

    Article Snippet: 6AN is an inhibitor of 6-PGDH, which was purchased from Cayman chemical company.

    Techniques: Marker

    Susceptibility to permethrin and DDT was increased in mosquitoes when pre-fed with 6AN. ( a ) In a permethrin susceptibility test, the G3 mosquitoes are susceptible to the diagnostic dose of permethrin (Per) (21.5 µg permethrin/bottle) (Mantel-Cox, P

    Journal: Scientific Reports

    Article Title: Redox state affects fecundity and insecticide susceptibility in Anopheles gambiae

    doi: 10.1038/s41598-018-31360-2

    Figure Lengend Snippet: Susceptibility to permethrin and DDT was increased in mosquitoes when pre-fed with 6AN. ( a ) In a permethrin susceptibility test, the G3 mosquitoes are susceptible to the diagnostic dose of permethrin (Per) (21.5 µg permethrin/bottle) (Mantel-Cox, P

    Article Snippet: 6AN is an inhibitor of 6-PGDH, which was purchased from Cayman chemical company.

    Techniques: Diagnostic Assay

    6AN and PQ target and off-target validation. ( a ) NADP + /NADPH ratio was elevated in 10 mM 6AN fed mosquitoes (Mann-Whitney, P = 0.0361). ( b ) ATP production was not changed between 10% sucrose fed mosquitoes and 0.1 mM PQ or 10 mM 6AN mosquitoes (One-way ANOVA, P = 0.7926). Error bars denote the standard deviation.

    Journal: Scientific Reports

    Article Title: Redox state affects fecundity and insecticide susceptibility in Anopheles gambiae

    doi: 10.1038/s41598-018-31360-2

    Figure Lengend Snippet: 6AN and PQ target and off-target validation. ( a ) NADP + /NADPH ratio was elevated in 10 mM 6AN fed mosquitoes (Mann-Whitney, P = 0.0361). ( b ) ATP production was not changed between 10% sucrose fed mosquitoes and 0.1 mM PQ or 10 mM 6AN mosquitoes (One-way ANOVA, P = 0.7926). Error bars denote the standard deviation.

    Article Snippet: 6AN is an inhibitor of 6-PGDH, which was purchased from Cayman chemical company.

    Techniques: MANN-WHITNEY, Standard Deviation

    Decreased egg number from PQ and 6AN stressed mosquitoes. Each point represents one female. Center bar represents the mean with standard deviation bar. The same sugar control group is used in both panels PQ ( a ) and 6AN ( b ). Oxidative stress induction reduced egg number (10 mM 6AN One-way ANOVA, P

    Journal: Scientific Reports

    Article Title: Redox state affects fecundity and insecticide susceptibility in Anopheles gambiae

    doi: 10.1038/s41598-018-31360-2

    Figure Lengend Snippet: Decreased egg number from PQ and 6AN stressed mosquitoes. Each point represents one female. Center bar represents the mean with standard deviation bar. The same sugar control group is used in both panels PQ ( a ) and 6AN ( b ). Oxidative stress induction reduced egg number (10 mM 6AN One-way ANOVA, P

    Article Snippet: 6AN is an inhibitor of 6-PGDH, which was purchased from Cayman chemical company.

    Techniques: Standard Deviation