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  • 99
    Thermo Fisher β mercaptoethanol
    Characterization of UVR8 G101S,W285A lines. a Dimer/monomer status of UVR8 from DSP-crosslinked extracts of various UVR8-overexpressing lines under a 35S or XVE-responsive promoter. UVR8 W285A - and XVE:UVR8 G101S,W285A -expressing lines were grown on 5 μM estradiol. Crosslinking was reversed by addition of 5% <t>β-mercaptoethanol.</t> UGPase is shown as loading control. b Representative images and quantification of hypocotyl length of seedlings of wild type (Ws), uvr8-7 , uvr8-7 /Pro 35S :UVR8 W285A (W285A-OX), and three independent lines each of uvr8-7 /Pro UVR8 :UVR8 W285A (#9, #21, and #23) and uvr8-7 /Pro UVR8 :UVR8 G101S,W285A (#1, #2, and #4) grown in darkness ( N > 60). Shared letters indicate no statistically significant difference in the means ( P
    β Mercaptoethanol, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 18833 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Millipore β nicotinamide adenine dinucleotide
    Metabolic instability of Jaspine B with rat liver microsomes. Jaspine B (1 μM) was incubated with 0.25 mg rat liver microsomes in the presence of a <t>β</t> -nicotinamide adenine dinucleotide 2′-phosphate reduced (NADPH)-generating system (1.3 mM β -NADP, 3.3 mM glucose-6-phosphate, 3.3 mM MgCl 2 , and 1.0 unit/mL glucose-6-phosphate dehydrogenase) for 60 min at 37 °C in a shaking water bath. The half-life (T 1/2 ) was calculated from the first-order degradation rate constant.
    β Nicotinamide Adenine Dinucleotide, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 526 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Millipore β nicotinamide adenine dinucleotide hydrate
    Exogenous NAD + (eNAD) rescues the galactose-induced reduction in cell viability and intracellular NAD + (iNAD) content in LS fibroblasts. a Dose-dependent effect of extracellular sodium pyruvate (10 mM), oxaloacetic acid (10 mM), dimethyl α-ketoglutarate (10 mM), 2-ketobutyric acid (10 mM), and l -aspartic acid (15 mM) on intracellular NAD (iNAD) levels in LS cells (24 h; N = 1, n = 3). b Dose-dependent effect of extracellular NAD (eNAD; <t>β-nicotinamide</t> adenine dinucleotide hydrate) on intracellular NAD (iNAD) levels (24 h; N = 1, n ≥ 6). c Dose-dependent rescue of the galactose-induced reduction in viability of LS cells (Calcein MSK images) by eNAD (β-nicotinamide adenine dinucleotide hydrate; S7 shown as a typical example; 96 h). d Quantification of the rescuing effect of eNAD in LS patient cells (96 h; N = 2 n ≥ 9). e Dose-dependent inhibition of the rescuing effect of eNAD by oleamide (OLE) in LS patient cells (96 h; N = 3, n = ≥ 6). Statistics: * P
    β Nicotinamide Adenine Dinucleotide Hydrate, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 105 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    96
    Millipore nadh
    Diagrammatic presentation of the mechanisms underlying the effects of <t>NAD</t> + on the intracellular adenylate pool of BV2 microglia under basal conditions.
    Nadh, supplied by Millipore, used in various techniques. Bioz Stars score: 96/100, based on 4930 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Millipore β nad nadh
    Diagrammatic presentation of the mechanisms underlying the effects of <t>NAD</t> + on the intracellular adenylate pool of BV2 microglia under basal conditions.
    β Nad Nadh, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    96
    Millipore β nicotinamide adenine dinucleotide 2 phosphate reduced tetrasodium salt hydrate nadph
    Activity of thioredoxin (Trx) system enzymes as measured by the 5,5′-dithiobis(2-nitrobenzoic acid) (DTNB) and insulin reduction assay. ( a ) Recovery of selenoenzyme thioredoxin reductase (TrxR, 20 nM) activity inhibited by methylmercury (MeHg, 200 nM) by the chelating agents [15]aneN 4 S, BAL and DMSA (40 µM) as measured by the DTNB reduction assay. ( b ) Recovery of Trx system activity by chelating agents ([15]aneN 4 S, BAL and DMSA; 40 µM) following incubation of TrxR (20 nM), Trx (3 µM) and <t>β-nicotinamide</t> adenine dinucleotide 2′-phosphate reduced <t>tetrasodium</t> salt hydrate <t>(NADPH)</t> with MeHg (200 nM) as measured by the insulin reduction assay. All data points represent the mean ± SE of at least three independent experiments. * Different from control, p
    β Nicotinamide Adenine Dinucleotide 2 Phosphate Reduced Tetrasodium Salt Hydrate Nadph, supplied by Millipore, used in various techniques. Bioz Stars score: 96/100, based on 91 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Millipore beta nicotinamide adenine dinucleotide
    Activity of thioredoxin (Trx) system enzymes as measured by the 5,5′-dithiobis(2-nitrobenzoic acid) (DTNB) and insulin reduction assay. ( a ) Recovery of selenoenzyme thioredoxin reductase (TrxR, 20 nM) activity inhibited by methylmercury (MeHg, 200 nM) by the chelating agents [15]aneN 4 S, BAL and DMSA (40 µM) as measured by the DTNB reduction assay. ( b ) Recovery of Trx system activity by chelating agents ([15]aneN 4 S, BAL and DMSA; 40 µM) following incubation of TrxR (20 nM), Trx (3 µM) and <t>β-nicotinamide</t> adenine dinucleotide 2′-phosphate reduced <t>tetrasodium</t> salt hydrate <t>(NADPH)</t> with MeHg (200 nM) as measured by the insulin reduction assay. All data points represent the mean ± SE of at least three independent experiments. * Different from control, p
    Beta Nicotinamide Adenine Dinucleotide, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 67 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    98
    Millipore nadph
    Activity of thioredoxin (Trx) system enzymes as measured by the 5,5′-dithiobis(2-nitrobenzoic acid) (DTNB) and insulin reduction assay. ( a ) Recovery of selenoenzyme thioredoxin reductase (TrxR, 20 nM) activity inhibited by methylmercury (MeHg, 200 nM) by the chelating agents [15]aneN 4 S, BAL and DMSA (40 µM) as measured by the DTNB reduction assay. ( b ) Recovery of Trx system activity by chelating agents ([15]aneN 4 S, BAL and DMSA; 40 µM) following incubation of TrxR (20 nM), Trx (3 µM) and <t>β-nicotinamide</t> adenine dinucleotide 2′-phosphate reduced <t>tetrasodium</t> salt hydrate <t>(NADPH)</t> with MeHg (200 nM) as measured by the insulin reduction assay. All data points represent the mean ± SE of at least three independent experiments. * Different from control, p
    Nadph, supplied by Millipore, used in various techniques. Bioz Stars score: 98/100, based on 3052 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    97
    Millipore β nicotinamide adenine dinucleotide 2 phosphate reduced tetrasodium salt nadph
    Activity of thioredoxin (Trx) system enzymes as measured by the 5,5′-dithiobis(2-nitrobenzoic acid) (DTNB) and insulin reduction assay. ( a ) Recovery of selenoenzyme thioredoxin reductase (TrxR, 20 nM) activity inhibited by methylmercury (MeHg, 200 nM) by the chelating agents [15]aneN 4 S, BAL and DMSA (40 µM) as measured by the DTNB reduction assay. ( b ) Recovery of Trx system activity by chelating agents ([15]aneN 4 S, BAL and DMSA; 40 µM) following incubation of TrxR (20 nM), Trx (3 µM) and <t>β-nicotinamide</t> adenine dinucleotide 2′-phosphate reduced <t>tetrasodium</t> salt hydrate <t>(NADPH)</t> with MeHg (200 nM) as measured by the insulin reduction assay. All data points represent the mean ± SE of at least three independent experiments. * Different from control, p
    β Nicotinamide Adenine Dinucleotide 2 Phosphate Reduced Tetrasodium Salt Nadph, supplied by Millipore, used in various techniques. Bioz Stars score: 97/100, based on 46 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Merck & Co β nicotinamide adenine dinucleotide
    Activity of thioredoxin (Trx) system enzymes as measured by the 5,5′-dithiobis(2-nitrobenzoic acid) (DTNB) and insulin reduction assay. ( a ) Recovery of selenoenzyme thioredoxin reductase (TrxR, 20 nM) activity inhibited by methylmercury (MeHg, 200 nM) by the chelating agents [15]aneN 4 S, BAL and DMSA (40 µM) as measured by the DTNB reduction assay. ( b ) Recovery of Trx system activity by chelating agents ([15]aneN 4 S, BAL and DMSA; 40 µM) following incubation of TrxR (20 nM), Trx (3 µM) and <t>β-nicotinamide</t> adenine dinucleotide 2′-phosphate reduced <t>tetrasodium</t> salt hydrate <t>(NADPH)</t> with MeHg (200 nM) as measured by the insulin reduction assay. All data points represent the mean ± SE of at least three independent experiments. * Different from control, p
    β Nicotinamide Adenine Dinucleotide, supplied by Merck & Co, used in various techniques. Bioz Stars score: 91/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    96
    Millipore β nicotinamide adenine dinucleotide sodium salt
    Activity of thioredoxin (Trx) system enzymes as measured by the 5,5′-dithiobis(2-nitrobenzoic acid) (DTNB) and insulin reduction assay. ( a ) Recovery of selenoenzyme thioredoxin reductase (TrxR, 20 nM) activity inhibited by methylmercury (MeHg, 200 nM) by the chelating agents [15]aneN 4 S, BAL and DMSA (40 µM) as measured by the DTNB reduction assay. ( b ) Recovery of Trx system activity by chelating agents ([15]aneN 4 S, BAL and DMSA; 40 µM) following incubation of TrxR (20 nM), Trx (3 µM) and <t>β-nicotinamide</t> adenine dinucleotide 2′-phosphate reduced <t>tetrasodium</t> salt hydrate <t>(NADPH)</t> with MeHg (200 nM) as measured by the insulin reduction assay. All data points represent the mean ± SE of at least three independent experiments. * Different from control, p
    β Nicotinamide Adenine Dinucleotide Sodium Salt, supplied by Millipore, used in various techniques. Bioz Stars score: 96/100, based on 30 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Millipore beta nicotinamide adenine dinucleotide 2 phosphate reduced tetrasodium salt hydrate
    Activity of thioredoxin (Trx) system enzymes as measured by the 5,5′-dithiobis(2-nitrobenzoic acid) (DTNB) and insulin reduction assay. ( a ) Recovery of selenoenzyme thioredoxin reductase (TrxR, 20 nM) activity inhibited by methylmercury (MeHg, 200 nM) by the chelating agents [15]aneN 4 S, BAL and DMSA (40 µM) as measured by the DTNB reduction assay. ( b ) Recovery of Trx system activity by chelating agents ([15]aneN 4 S, BAL and DMSA; 40 µM) following incubation of TrxR (20 nM), Trx (3 µM) and <t>β-nicotinamide</t> adenine dinucleotide 2′-phosphate reduced <t>tetrasodium</t> salt hydrate <t>(NADPH)</t> with MeHg (200 nM) as measured by the insulin reduction assay. All data points represent the mean ± SE of at least three independent experiments. * Different from control, p
    Beta Nicotinamide Adenine Dinucleotide 2 Phosphate Reduced Tetrasodium Salt Hydrate, supplied by Millipore, used in various techniques. Bioz Stars score: 94/100, based on 28 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Carl Roth GmbH β nicotinamide adenine dinucleotide
    Activity of thioredoxin (Trx) system enzymes as measured by the 5,5′-dithiobis(2-nitrobenzoic acid) (DTNB) and insulin reduction assay. ( a ) Recovery of selenoenzyme thioredoxin reductase (TrxR, 20 nM) activity inhibited by methylmercury (MeHg, 200 nM) by the chelating agents [15]aneN 4 S, BAL and DMSA (40 µM) as measured by the DTNB reduction assay. ( b ) Recovery of Trx system activity by chelating agents ([15]aneN 4 S, BAL and DMSA; 40 µM) following incubation of TrxR (20 nM), Trx (3 µM) and <t>β-nicotinamide</t> adenine dinucleotide 2′-phosphate reduced <t>tetrasodium</t> salt hydrate <t>(NADPH)</t> with MeHg (200 nM) as measured by the insulin reduction assay. All data points represent the mean ± SE of at least three independent experiments. * Different from control, p
    β Nicotinamide Adenine Dinucleotide, supplied by Carl Roth GmbH, used in various techniques. Bioz Stars score: 91/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Nacalai β nad
    Activity of thioredoxin (Trx) system enzymes as measured by the 5,5′-dithiobis(2-nitrobenzoic acid) (DTNB) and insulin reduction assay. ( a ) Recovery of selenoenzyme thioredoxin reductase (TrxR, 20 nM) activity inhibited by methylmercury (MeHg, 200 nM) by the chelating agents [15]aneN 4 S, BAL and DMSA (40 µM) as measured by the DTNB reduction assay. ( b ) Recovery of Trx system activity by chelating agents ([15]aneN 4 S, BAL and DMSA; 40 µM) following incubation of TrxR (20 nM), Trx (3 µM) and <t>β-nicotinamide</t> adenine dinucleotide 2′-phosphate reduced <t>tetrasodium</t> salt hydrate <t>(NADPH)</t> with MeHg (200 nM) as measured by the insulin reduction assay. All data points represent the mean ± SE of at least three independent experiments. * Different from control, p
    β Nad, supplied by Nacalai, used in various techniques. Bioz Stars score: 93/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Characterization of UVR8 G101S,W285A lines. a Dimer/monomer status of UVR8 from DSP-crosslinked extracts of various UVR8-overexpressing lines under a 35S or XVE-responsive promoter. UVR8 W285A - and XVE:UVR8 G101S,W285A -expressing lines were grown on 5 μM estradiol. Crosslinking was reversed by addition of 5% β-mercaptoethanol. UGPase is shown as loading control. b Representative images and quantification of hypocotyl length of seedlings of wild type (Ws), uvr8-7 , uvr8-7 /Pro 35S :UVR8 W285A (W285A-OX), and three independent lines each of uvr8-7 /Pro UVR8 :UVR8 W285A (#9, #21, and #23) and uvr8-7 /Pro UVR8 :UVR8 G101S,W285A (#1, #2, and #4) grown in darkness ( N > 60). Shared letters indicate no statistically significant difference in the means ( P

    Journal: bioRxiv

    Article Title: A constitutively monomeric UVR8 photoreceptor allele confers enhanced UV-B photomorphogenesis

    doi: 10.1101/2020.08.02.233007

    Figure Lengend Snippet: Characterization of UVR8 G101S,W285A lines. a Dimer/monomer status of UVR8 from DSP-crosslinked extracts of various UVR8-overexpressing lines under a 35S or XVE-responsive promoter. UVR8 W285A - and XVE:UVR8 G101S,W285A -expressing lines were grown on 5 μM estradiol. Crosslinking was reversed by addition of 5% β-mercaptoethanol. UGPase is shown as loading control. b Representative images and quantification of hypocotyl length of seedlings of wild type (Ws), uvr8-7 , uvr8-7 /Pro 35S :UVR8 W285A (W285A-OX), and three independent lines each of uvr8-7 /Pro UVR8 :UVR8 W285A (#9, #21, and #23) and uvr8-7 /Pro UVR8 :UVR8 G101S,W285A (#1, #2, and #4) grown in darkness ( N > 60). Shared letters indicate no statistically significant difference in the means ( P

    Article Snippet: To reverse crosslinking, 5% [v/v] β-mercaptoethanol was added prior to heat-based denaturation.

    Techniques: Expressing

    Metabolic instability of Jaspine B with rat liver microsomes. Jaspine B (1 μM) was incubated with 0.25 mg rat liver microsomes in the presence of a β -nicotinamide adenine dinucleotide 2′-phosphate reduced (NADPH)-generating system (1.3 mM β -NADP, 3.3 mM glucose-6-phosphate, 3.3 mM MgCl 2 , and 1.0 unit/mL glucose-6-phosphate dehydrogenase) for 60 min at 37 °C in a shaking water bath. The half-life (T 1/2 ) was calculated from the first-order degradation rate constant.

    Journal: Marine Drugs

    Article Title: Pharmacokinetics of Jaspine B and Enhancement of Intestinal Absorption of Jaspine B in the Presence of Bile Acid in Rats

    doi: 10.3390/md15090279

    Figure Lengend Snippet: Metabolic instability of Jaspine B with rat liver microsomes. Jaspine B (1 μM) was incubated with 0.25 mg rat liver microsomes in the presence of a β -nicotinamide adenine dinucleotide 2′-phosphate reduced (NADPH)-generating system (1.3 mM β -NADP, 3.3 mM glucose-6-phosphate, 3.3 mM MgCl 2 , and 1.0 unit/mL glucose-6-phosphate dehydrogenase) for 60 min at 37 °C in a shaking water bath. The half-life (T 1/2 ) was calculated from the first-order degradation rate constant.

    Article Snippet: Hank’s balanced salt solution (HBSS), taurocholate (TC), Lucifer yellow, dimethyl sulfoxide (DMSO), polyethylene glycol (PEG) 400, β -nicotinamide adenine dinucleotide (β -NAD), 3α-hydroxysteroid dehyrogenase (3α-HSD), EDTA, and Tris base were purchased from Sigma-Aldrich (St. Louis, MO, USA).

    Techniques: Incubation

    Hyperpolarization to β-NAD and ADPR is absent in P2ry1 −/− colons

    Journal: The Journal of Physiology

    Article Title: P2Y1 purinoreceptors are fundamental to inhibitory motor control of murine colonic excitability and transit

    doi: 10.1113/jphysiol.2011.224634

    Figure Lengend Snippet: Hyperpolarization to β-NAD and ADPR is absent in P2ry1 −/− colons

    Article Snippet: Adenosine-5′-triphosphate (ATP), adenosine 5′-diphosphate (ADP), β-nicotinamide adenine dinucleotide (β-NAD), adenosine diphosphate ribose (ADPR), tetrodotoxin (TTX), atropine, Nω-Nitro- l -arginine ( l -NNA) and apamin were purchased from Sigma-Aldrich (St Louis, MO, USA).

    Techniques:

    Hyperpolarization responses to β-NAD and ADPR in wild-type and P2ry1 −/− colons in the presence of atropine and l -NNA

    Journal: The Journal of Physiology

    Article Title: P2Y1 purinoreceptors are fundamental to inhibitory motor control of murine colonic excitability and transit

    doi: 10.1113/jphysiol.2011.224634

    Figure Lengend Snippet: Hyperpolarization responses to β-NAD and ADPR in wild-type and P2ry1 −/− colons in the presence of atropine and l -NNA

    Article Snippet: Adenosine-5′-triphosphate (ATP), adenosine 5′-diphosphate (ADP), β-nicotinamide adenine dinucleotide (β-NAD), adenosine diphosphate ribose (ADPR), tetrodotoxin (TTX), atropine, Nω-Nitro- l -arginine ( l -NNA) and apamin were purchased from Sigma-Aldrich (St Louis, MO, USA).

    Techniques:

    Relaxation responses to ATP and β-NAD in wild-type and P2ry1 −/− colons

    Journal: The Journal of Physiology

    Article Title: P2Y1 purinoreceptors are fundamental to inhibitory motor control of murine colonic excitability and transit

    doi: 10.1113/jphysiol.2011.224634

    Figure Lengend Snippet: Relaxation responses to ATP and β-NAD in wild-type and P2ry1 −/− colons

    Article Snippet: Adenosine-5′-triphosphate (ATP), adenosine 5′-diphosphate (ADP), β-nicotinamide adenine dinucleotide (β-NAD), adenosine diphosphate ribose (ADPR), tetrodotoxin (TTX), atropine, Nω-Nitro- l -arginine ( l -NNA) and apamin were purchased from Sigma-Aldrich (St Louis, MO, USA).

    Techniques:

    Exogenous NAD + (eNAD) rescues the galactose-induced reduction in cell viability and intracellular NAD + (iNAD) content in LS fibroblasts. a Dose-dependent effect of extracellular sodium pyruvate (10 mM), oxaloacetic acid (10 mM), dimethyl α-ketoglutarate (10 mM), 2-ketobutyric acid (10 mM), and l -aspartic acid (15 mM) on intracellular NAD (iNAD) levels in LS cells (24 h; N = 1, n = 3). b Dose-dependent effect of extracellular NAD (eNAD; β-nicotinamide adenine dinucleotide hydrate) on intracellular NAD (iNAD) levels (24 h; N = 1, n ≥ 6). c Dose-dependent rescue of the galactose-induced reduction in viability of LS cells (Calcein MSK images) by eNAD (β-nicotinamide adenine dinucleotide hydrate; S7 shown as a typical example; 96 h). d Quantification of the rescuing effect of eNAD in LS patient cells (96 h; N = 2 n ≥ 9). e Dose-dependent inhibition of the rescuing effect of eNAD by oleamide (OLE) in LS patient cells (96 h; N = 3, n = ≥ 6). Statistics: * P

    Journal: Cell Death & Disease

    Article Title: Rescue from galactose-induced death of Leigh Syndrome patient cells by pyruvate and NAD+

    doi: 10.1038/s41419-018-1179-4

    Figure Lengend Snippet: Exogenous NAD + (eNAD) rescues the galactose-induced reduction in cell viability and intracellular NAD + (iNAD) content in LS fibroblasts. a Dose-dependent effect of extracellular sodium pyruvate (10 mM), oxaloacetic acid (10 mM), dimethyl α-ketoglutarate (10 mM), 2-ketobutyric acid (10 mM), and l -aspartic acid (15 mM) on intracellular NAD (iNAD) levels in LS cells (24 h; N = 1, n = 3). b Dose-dependent effect of extracellular NAD (eNAD; β-nicotinamide adenine dinucleotide hydrate) on intracellular NAD (iNAD) levels (24 h; N = 1, n ≥ 6). c Dose-dependent rescue of the galactose-induced reduction in viability of LS cells (Calcein MSK images) by eNAD (β-nicotinamide adenine dinucleotide hydrate; S7 shown as a typical example; 96 h). d Quantification of the rescuing effect of eNAD in LS patient cells (96 h; N = 2 n ≥ 9). e Dose-dependent inhibition of the rescuing effect of eNAD by oleamide (OLE) in LS patient cells (96 h; N = 3, n = ≥ 6). Statistics: * P

    Article Snippet: Medium additions In certain experiments (one of) the following compounds was/were added to the medium: sodium pyruvate (#11360070, Life Technologies, Carlsbad, CA, USA), l -aspartic acid (#A7219, Sigma-Aldrich), 2-ketobutyric acid (#K401, Sigma-Aldrich), oxaloacetic acid (#O4126, Sigma-Aldrich), sodium l -lactate (#L7022, Sigma-Aldrich), l -(-)-malic acid (#M1000, Sigma-Aldrich), sodium succinate dibasic hexahydrate (#S9637, Sigma-Aldrich), dimethyl α-ketoglutarate (#349631, Sigma-Aldrich), uridine (#U3003, Sigma-Aldrich), β-nicotinamide adenine dinucleotide hydrate (#43410, Sigma-Aldrich), Oleamide (#O2136, Sigma-Aldrich) These compounds were dissolved directly in the medium after which its pH was adjusted to 7.2 with NaOH.

    Techniques: Inhibition

    Diagrammatic presentation of the mechanisms underlying the effects of NAD + on the intracellular adenylate pool of BV2 microglia under basal conditions.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Extracellular Degradation Into Adenosine and the Activities of Adenosine Kinase and AMPK Mediate Extracellular NAD+-Produced Increases in the Adenylate Pool of BV2 Microglia Under Basal Conditions

    doi: 10.3389/fncel.2018.00343

    Figure Lengend Snippet: Diagrammatic presentation of the mechanisms underlying the effects of NAD + on the intracellular adenylate pool of BV2 microglia under basal conditions.

    Article Snippet: NADH (N4505), NAD+ (N0632), dorsomorhpin (P5499), Adenosine 5′-monophosphate (AMP, 01930), pyridoxyl phosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS, P178), 5-Iodotubercidin (I-100) and dipyridamole (DPR, D9766) were purchased from Sigma Aldrich (St. Louis, MO, United States).

    Techniques:

    Adenosine uptake plays a key role in the NAD + -induced increases in the intracellular levels of ATP, ADP, and AMP of BV2 microglia under basal conditions. (A) NAD + dose-dependently increased the extracellular adenosine level of BV2 cells. The cells were treated with NAD + for 3 h. (B) Time course of 500 μM NAD + -induced increases in the extracellular adenosine levels of BV2 cells. (C) Treatment of the cells with 0.5 μM DPR completely blocked the NAD + -induced increases in the intracellular ATP levels of the cells. (D) Treatment of the cells with 0.5 μM DPR completely blocked the NAD + -induced increases in the intracellular ADP levels of the cells. (E) Treatment of the cells with 0.5 μM DPR completely blocked the NAD + -induced increases in the intracellular AMP levels of the cells. The cells were co-treated with NAD + and DPR for 3 h. Subsequently, the assays on intracellular ATP, ADP, and AMP levels were conducted. N = 16. The data were pooled from four independent experiments. ∗ P

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Extracellular Degradation Into Adenosine and the Activities of Adenosine Kinase and AMPK Mediate Extracellular NAD+-Produced Increases in the Adenylate Pool of BV2 Microglia Under Basal Conditions

    doi: 10.3389/fncel.2018.00343

    Figure Lengend Snippet: Adenosine uptake plays a key role in the NAD + -induced increases in the intracellular levels of ATP, ADP, and AMP of BV2 microglia under basal conditions. (A) NAD + dose-dependently increased the extracellular adenosine level of BV2 cells. The cells were treated with NAD + for 3 h. (B) Time course of 500 μM NAD + -induced increases in the extracellular adenosine levels of BV2 cells. (C) Treatment of the cells with 0.5 μM DPR completely blocked the NAD + -induced increases in the intracellular ATP levels of the cells. (D) Treatment of the cells with 0.5 μM DPR completely blocked the NAD + -induced increases in the intracellular ADP levels of the cells. (E) Treatment of the cells with 0.5 μM DPR completely blocked the NAD + -induced increases in the intracellular AMP levels of the cells. The cells were co-treated with NAD + and DPR for 3 h. Subsequently, the assays on intracellular ATP, ADP, and AMP levels were conducted. N = 16. The data were pooled from four independent experiments. ∗ P

    Article Snippet: NADH (N4505), NAD+ (N0632), dorsomorhpin (P5499), Adenosine 5′-monophosphate (AMP, 01930), pyridoxyl phosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS, P178), 5-Iodotubercidin (I-100) and dipyridamole (DPR, D9766) were purchased from Sigma Aldrich (St. Louis, MO, United States).

    Techniques:

    NAD + treatment increased AMPK phosphorylation of BV2 microglia under basal conditions. (A) Both 100 and 500 μM NAD + increased AMPK phosphorylation. (B) NAD + treatment increased ACC phosphorylation. (C) 5 μM 5-ITU blocked the NAD + -induced AMPK phosphorylation in BV2 microglia. (D) NAD + treatment did not affect the AMP/ATP ratios of the cells. The cells were treated with NAD + for 0.5 h. N = 12. The data were pooled from four independent experiments. ∗ P

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Extracellular Degradation Into Adenosine and the Activities of Adenosine Kinase and AMPK Mediate Extracellular NAD+-Produced Increases in the Adenylate Pool of BV2 Microglia Under Basal Conditions

    doi: 10.3389/fncel.2018.00343

    Figure Lengend Snippet: NAD + treatment increased AMPK phosphorylation of BV2 microglia under basal conditions. (A) Both 100 and 500 μM NAD + increased AMPK phosphorylation. (B) NAD + treatment increased ACC phosphorylation. (C) 5 μM 5-ITU blocked the NAD + -induced AMPK phosphorylation in BV2 microglia. (D) NAD + treatment did not affect the AMP/ATP ratios of the cells. The cells were treated with NAD + for 0.5 h. N = 12. The data were pooled from four independent experiments. ∗ P

    Article Snippet: NADH (N4505), NAD+ (N0632), dorsomorhpin (P5499), Adenosine 5′-monophosphate (AMP, 01930), pyridoxyl phosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS, P178), 5-Iodotubercidin (I-100) and dipyridamole (DPR, D9766) were purchased from Sigma Aldrich (St. Louis, MO, United States).

    Techniques:

    Adenosine kinase mediates the NAD + -induced increases in the intracellular levels of ATP, ADP, and AMP of BV2 microglia under basal conditions. (A) NAD + treatment dose-dependently increased the intracellular adenosine level of the cells. (B) 500 μM NAD + time-dependently increased the intracellular adenosine level of BV2 cells. (C) Treatment of the cells with 5 μM 5-ITU blocked the NAD + -induced increases in the intracellular ATP levels of the cells. (D) Treatment of the cells with 5 μM 5-ITU blocked the NAD + - induced increases in the intracellular ADP levels of the cells. (E) Treatment of the cells with 5 μM 5-ITU blocked the NAD + -induced increases in the intracellular AMP levels of the cells. The cells were co-treated with 5 μM 5-ITU and NAD + for 3 h before the assays were conducted. N = 16. The data were pooled from four independent experiments. ∗∗∗ P

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Extracellular Degradation Into Adenosine and the Activities of Adenosine Kinase and AMPK Mediate Extracellular NAD+-Produced Increases in the Adenylate Pool of BV2 Microglia Under Basal Conditions

    doi: 10.3389/fncel.2018.00343

    Figure Lengend Snippet: Adenosine kinase mediates the NAD + -induced increases in the intracellular levels of ATP, ADP, and AMP of BV2 microglia under basal conditions. (A) NAD + treatment dose-dependently increased the intracellular adenosine level of the cells. (B) 500 μM NAD + time-dependently increased the intracellular adenosine level of BV2 cells. (C) Treatment of the cells with 5 μM 5-ITU blocked the NAD + -induced increases in the intracellular ATP levels of the cells. (D) Treatment of the cells with 5 μM 5-ITU blocked the NAD + - induced increases in the intracellular ADP levels of the cells. (E) Treatment of the cells with 5 μM 5-ITU blocked the NAD + -induced increases in the intracellular AMP levels of the cells. The cells were co-treated with 5 μM 5-ITU and NAD + for 3 h before the assays were conducted. N = 16. The data were pooled from four independent experiments. ∗∗∗ P

    Article Snippet: NADH (N4505), NAD+ (N0632), dorsomorhpin (P5499), Adenosine 5′-monophosphate (AMP, 01930), pyridoxyl phosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS, P178), 5-Iodotubercidin (I-100) and dipyridamole (DPR, D9766) were purchased from Sigma Aldrich (St. Louis, MO, United States).

    Techniques:

    AMPK mediated the NAD + -induced increases in the intracellular ATP levels of BV2 microglia under basal conditions. (A) Dorsomorphin, an AMPK inhibitor, prevented NAD + - induced ATP increases in BV2 cells. The cells were co-treated with 15 μM dorsomorphin and NAD + for 3 h before the ATP assay were conducted. (B) AMPK siRNA treatment led to a significant decrease in the AMPK protein level of BV2 cells. (C) AMPK siRNA significantly attenuated the NAD + -induced ATP increases of BV2 cells. The cells were pretreated with AMPK siRNA for 24 h. Subsequently, the cells were treated with NAD + for 3 h. N = 12. The data were pooled from four independent experiments. ∗ P

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Extracellular Degradation Into Adenosine and the Activities of Adenosine Kinase and AMPK Mediate Extracellular NAD+-Produced Increases in the Adenylate Pool of BV2 Microglia Under Basal Conditions

    doi: 10.3389/fncel.2018.00343

    Figure Lengend Snippet: AMPK mediated the NAD + -induced increases in the intracellular ATP levels of BV2 microglia under basal conditions. (A) Dorsomorphin, an AMPK inhibitor, prevented NAD + - induced ATP increases in BV2 cells. The cells were co-treated with 15 μM dorsomorphin and NAD + for 3 h before the ATP assay were conducted. (B) AMPK siRNA treatment led to a significant decrease in the AMPK protein level of BV2 cells. (C) AMPK siRNA significantly attenuated the NAD + -induced ATP increases of BV2 cells. The cells were pretreated with AMPK siRNA for 24 h. Subsequently, the cells were treated with NAD + for 3 h. N = 12. The data were pooled from four independent experiments. ∗ P

    Article Snippet: NADH (N4505), NAD+ (N0632), dorsomorhpin (P5499), Adenosine 5′-monophosphate (AMP, 01930), pyridoxyl phosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS, P178), 5-Iodotubercidin (I-100) and dipyridamole (DPR, D9766) were purchased from Sigma Aldrich (St. Louis, MO, United States).

    Techniques: ATP Assay

    Effects of NAD + treatment on the intracellular levels of ATP, ADP, and AMP of BV2 microglia under basal conditions. (A) NAD + treatment significantly increased the intracellular ATP level of the cells. (B) NAD + treatment significantly increased the intracellular ADP level of the cells. (C) NAD + treatment significantly increased the intracellular AMP level of the cells. (D) NAD + treatment significantly increased the intracellular NAD + level of the cells. (E) NAD + (500 μM) time-dependently increased the intracellular ATP level of the cells. (F) NAD + (500 μM) time-dependently increased the intracellular ADP level of the cells. (G) NAD + (500 μM) time-dependently increased the intracellular AMP level of the cells. (H) NAD + (500 μM) treatment did not alter the ADP/ATP ratio. (I) NAD + (500 μM) did not alter the AMP/ATP ratio. For (A–C) , BV2 cells were treated with NAD + for 3 h before the assays were conducted. N = 16. The data were pooled from four independent experiments. ∗ P

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Extracellular Degradation Into Adenosine and the Activities of Adenosine Kinase and AMPK Mediate Extracellular NAD+-Produced Increases in the Adenylate Pool of BV2 Microglia Under Basal Conditions

    doi: 10.3389/fncel.2018.00343

    Figure Lengend Snippet: Effects of NAD + treatment on the intracellular levels of ATP, ADP, and AMP of BV2 microglia under basal conditions. (A) NAD + treatment significantly increased the intracellular ATP level of the cells. (B) NAD + treatment significantly increased the intracellular ADP level of the cells. (C) NAD + treatment significantly increased the intracellular AMP level of the cells. (D) NAD + treatment significantly increased the intracellular NAD + level of the cells. (E) NAD + (500 μM) time-dependently increased the intracellular ATP level of the cells. (F) NAD + (500 μM) time-dependently increased the intracellular ADP level of the cells. (G) NAD + (500 μM) time-dependently increased the intracellular AMP level of the cells. (H) NAD + (500 μM) treatment did not alter the ADP/ATP ratio. (I) NAD + (500 μM) did not alter the AMP/ATP ratio. For (A–C) , BV2 cells were treated with NAD + for 3 h before the assays were conducted. N = 16. The data were pooled from four independent experiments. ∗ P

    Article Snippet: NADH (N4505), NAD+ (N0632), dorsomorhpin (P5499), Adenosine 5′-monophosphate (AMP, 01930), pyridoxyl phosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS, P178), 5-Iodotubercidin (I-100) and dipyridamole (DPR, D9766) were purchased from Sigma Aldrich (St. Louis, MO, United States).

    Techniques:

    Activity of thioredoxin (Trx) system enzymes as measured by the 5,5′-dithiobis(2-nitrobenzoic acid) (DTNB) and insulin reduction assay. ( a ) Recovery of selenoenzyme thioredoxin reductase (TrxR, 20 nM) activity inhibited by methylmercury (MeHg, 200 nM) by the chelating agents [15]aneN 4 S, BAL and DMSA (40 µM) as measured by the DTNB reduction assay. ( b ) Recovery of Trx system activity by chelating agents ([15]aneN 4 S, BAL and DMSA; 40 µM) following incubation of TrxR (20 nM), Trx (3 µM) and β-nicotinamide adenine dinucleotide 2′-phosphate reduced tetrasodium salt hydrate (NADPH) with MeHg (200 nM) as measured by the insulin reduction assay. All data points represent the mean ± SE of at least three independent experiments. * Different from control, p

    Journal: International Journal of Environmental Research and Public Health

    Article Title: In Vitro Assessment of the Efficacy of a Macrocyclic Chelator in Reversing Methylmercury Toxicity

    doi: 10.3390/ijerph16234817

    Figure Lengend Snippet: Activity of thioredoxin (Trx) system enzymes as measured by the 5,5′-dithiobis(2-nitrobenzoic acid) (DTNB) and insulin reduction assay. ( a ) Recovery of selenoenzyme thioredoxin reductase (TrxR, 20 nM) activity inhibited by methylmercury (MeHg, 200 nM) by the chelating agents [15]aneN 4 S, BAL and DMSA (40 µM) as measured by the DTNB reduction assay. ( b ) Recovery of Trx system activity by chelating agents ([15]aneN 4 S, BAL and DMSA; 40 µM) following incubation of TrxR (20 nM), Trx (3 µM) and β-nicotinamide adenine dinucleotide 2′-phosphate reduced tetrasodium salt hydrate (NADPH) with MeHg (200 nM) as measured by the insulin reduction assay. All data points represent the mean ± SE of at least three independent experiments. * Different from control, p

    Article Snippet: Reagents Methylmercury chloride (CH3 HgCl), dithiothreitol (DTT), 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide (MTT), 5,5′-dithiobis(2-nitrobenzoic acid) (DTNB), β-nicotinamide adenine dinucleotide 2′-phosphate reduced tetrasodium salt hydrate (NADPH), insulin (human recombinant), BAL and DMSA were purchased from Sigma-Aldrich.

    Techniques: Activity Assay, Insulin Reduction Assay, Incubation