atp based celltiter glo luminescent cell viability kit  (Promega)

 
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    Promega atp based celltiter glo luminescent cell viability kit
    Cultured primary neurons derived from ALDH2*2/*2 mice are more sensitive to ethanol-induced toxicity relative to primary neurons of WT mice. a ) LDH release a measure of cell death, was determined using LDH assay kit in primary neurons in the presence or absence of Alda-1 (20 μM/48 h) and ethanol (50 mM); Veh – Vehicle; A – Alda-1. b ) Cellular ROS production was determined using 2,7 dichloro- fluorescein diacetate (DCFDA) in primary neurons, treated as in a; Veh – Vehicle; A – Alda-1. c ) Measurement of cellular <t>ATP</t> levels using <t>CellTiter-Glo</t> Luminescent Cell Viability kit; Veh – Vehicle; A – Alda-1. d ) Quantitation of basal respiration (OCR) as a measure of oxidative phosphorylation (OXPHOS) using Seahorse Extracellular Flux in primary neurons treated as in a; Veh – Vehicle; A – Alda-1. e ) Quantitation of extracellular acidification rate (ECAR) as a measure of glycolytic dependence using Seahorse Extracellular Flux in primary neuron, treated as in a; Veh – Vehicle; A – Alda-1. f ) Levels of LC3B, TOM20, p53 and phosphorylation of JNK (Thr183/Tyr185) were determined in primary neurons, treated as in a, by immunoblotting. β-actin was used as loading control; Veh – Vehicle; A – Alda-1. Data information: Mean, standard deviation, and p-values are shown. Results are presented as percent/ fold of control. n = 3–4 independent biological replicates; probability by one-way ANOVA (with Holm-Sidak post hoc test)
    Atp Based Celltiter Glo Luminescent Cell Viability Kit, supplied by Promega, used in various techniques. Bioz Stars score: 92/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/atp based celltiter glo luminescent cell viability kit/product/Promega
    Average 92 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    atp based celltiter glo luminescent cell viability kit - by Bioz Stars, 2020-03
    92/100 stars

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    1) Product Images from "Aldehyde dehydrogenase 2 activity and aldehydic load contribute to neuroinflammation and Alzheimer’s disease related pathology"

    Article Title: Aldehyde dehydrogenase 2 activity and aldehydic load contribute to neuroinflammation and Alzheimer’s disease related pathology

    Journal: Acta Neuropathologica Communications

    doi: 10.1186/s40478-019-0839-7

    Cultured primary neurons derived from ALDH2*2/*2 mice are more sensitive to ethanol-induced toxicity relative to primary neurons of WT mice. a ) LDH release a measure of cell death, was determined using LDH assay kit in primary neurons in the presence or absence of Alda-1 (20 μM/48 h) and ethanol (50 mM); Veh – Vehicle; A – Alda-1. b ) Cellular ROS production was determined using 2,7 dichloro- fluorescein diacetate (DCFDA) in primary neurons, treated as in a; Veh – Vehicle; A – Alda-1. c ) Measurement of cellular ATP levels using CellTiter-Glo Luminescent Cell Viability kit; Veh – Vehicle; A – Alda-1. d ) Quantitation of basal respiration (OCR) as a measure of oxidative phosphorylation (OXPHOS) using Seahorse Extracellular Flux in primary neurons treated as in a; Veh – Vehicle; A – Alda-1. e ) Quantitation of extracellular acidification rate (ECAR) as a measure of glycolytic dependence using Seahorse Extracellular Flux in primary neuron, treated as in a; Veh – Vehicle; A – Alda-1. f ) Levels of LC3B, TOM20, p53 and phosphorylation of JNK (Thr183/Tyr185) were determined in primary neurons, treated as in a, by immunoblotting. β-actin was used as loading control; Veh – Vehicle; A – Alda-1. Data information: Mean, standard deviation, and p-values are shown. Results are presented as percent/ fold of control. n = 3–4 independent biological replicates; probability by one-way ANOVA (with Holm-Sidak post hoc test)
    Figure Legend Snippet: Cultured primary neurons derived from ALDH2*2/*2 mice are more sensitive to ethanol-induced toxicity relative to primary neurons of WT mice. a ) LDH release a measure of cell death, was determined using LDH assay kit in primary neurons in the presence or absence of Alda-1 (20 μM/48 h) and ethanol (50 mM); Veh – Vehicle; A – Alda-1. b ) Cellular ROS production was determined using 2,7 dichloro- fluorescein diacetate (DCFDA) in primary neurons, treated as in a; Veh – Vehicle; A – Alda-1. c ) Measurement of cellular ATP levels using CellTiter-Glo Luminescent Cell Viability kit; Veh – Vehicle; A – Alda-1. d ) Quantitation of basal respiration (OCR) as a measure of oxidative phosphorylation (OXPHOS) using Seahorse Extracellular Flux in primary neurons treated as in a; Veh – Vehicle; A – Alda-1. e ) Quantitation of extracellular acidification rate (ECAR) as a measure of glycolytic dependence using Seahorse Extracellular Flux in primary neuron, treated as in a; Veh – Vehicle; A – Alda-1. f ) Levels of LC3B, TOM20, p53 and phosphorylation of JNK (Thr183/Tyr185) were determined in primary neurons, treated as in a, by immunoblotting. β-actin was used as loading control; Veh – Vehicle; A – Alda-1. Data information: Mean, standard deviation, and p-values are shown. Results are presented as percent/ fold of control. n = 3–4 independent biological replicates; probability by one-way ANOVA (with Holm-Sidak post hoc test)

    Techniques Used: Cell Culture, Derivative Assay, Mouse Assay, Lactate Dehydrogenase Assay, Quantitation Assay, Standard Deviation

    Cultured primary astrocyte derived from ALDH2*2/*2 mice are more activated in response to ethanol relative to primary astrocytes of WT mice. a ) Measurement of mitochondrial ROS using MitoSOX™ in primary astrocytes in the presence or absence of Alda-1 (20 μM/24 h; 50 mM Ethanol); Veh – Vehicle; A – Alda-1. b ) Heat map representation of qPCR analysis of genes associated with inflammation, apoptosis, autophagy and mitochondrial health; Veh – Vehicle; A – Alda-1. c ) Nitrite levels were determined in primary astrocytes using Griess reagent kit in the presence or absence of Alda-1 (20 μM/24 h; 50 mM Ethanol); Veh – Vehicle; A – Alda-1. d ) Measurement of cellular ATP levels using CellTiter-Glo Luminescent Cell Viability kit in primary astrocytes in the presence or absence of Alda-1 (20 μM/24 h; 50 mM Ethanol); Veh – Vehicle; A – Alda-1. e ) Levels of cellular COX-2 and interleukin-1β release at 6 h were determined by immunoblotting in primary astrocytes in the presence or absence of Alda-1 (20 μM; 50 mM Ethanol). β-actin was used as loading control; Veh – Vehicle; A – Alda-1. Data information: Mean, standard deviation, and p-values are shown. Results are presented as fold of control. n = 3–4 independent biological replicates; probability by one-way ANOVA (with Holm-Sidak post hoc test)
    Figure Legend Snippet: Cultured primary astrocyte derived from ALDH2*2/*2 mice are more activated in response to ethanol relative to primary astrocytes of WT mice. a ) Measurement of mitochondrial ROS using MitoSOX™ in primary astrocytes in the presence or absence of Alda-1 (20 μM/24 h; 50 mM Ethanol); Veh – Vehicle; A – Alda-1. b ) Heat map representation of qPCR analysis of genes associated with inflammation, apoptosis, autophagy and mitochondrial health; Veh – Vehicle; A – Alda-1. c ) Nitrite levels were determined in primary astrocytes using Griess reagent kit in the presence or absence of Alda-1 (20 μM/24 h; 50 mM Ethanol); Veh – Vehicle; A – Alda-1. d ) Measurement of cellular ATP levels using CellTiter-Glo Luminescent Cell Viability kit in primary astrocytes in the presence or absence of Alda-1 (20 μM/24 h; 50 mM Ethanol); Veh – Vehicle; A – Alda-1. e ) Levels of cellular COX-2 and interleukin-1β release at 6 h were determined by immunoblotting in primary astrocytes in the presence or absence of Alda-1 (20 μM; 50 mM Ethanol). β-actin was used as loading control; Veh – Vehicle; A – Alda-1. Data information: Mean, standard deviation, and p-values are shown. Results are presented as fold of control. n = 3–4 independent biological replicates; probability by one-way ANOVA (with Holm-Sidak post hoc test)

    Techniques Used: Cell Culture, Derivative Assay, Mouse Assay, Real-time Polymerase Chain Reaction, Standard Deviation

    ALDH2*2 mutation is associated with increased oxidative stress in patient-derived fibroblasts with familial Alzheimer’s Disease (AD). a ) Genotyping of a Japanese AD patient-derived fibroblasts identifies heterozygous ALDH2*2/*1 mutation. ALDH2 protein expression in these cells was measured by immunoblotting three different culture passage numbers. b ) The levels of ALDH2 protein were determined in total lysates by immunoblotting of control (healthy subject; H)- and 2*2/*1 AD patient-derived fibroblasts. β-actin was used as loading control. c ) ALDH2 protein levels were quantified and represented as fold change of control. d ) Enzymatic activity of ALDH2 in lysates from ALDH2*2/*1 AD patient-derived fibroblasts relative to fibroblasts from control was measured over 5 min. e ) 4-HNE levels in control and AD patient-derived fibroblasts were measured using 4-HNE assay kit in the presence or absence of Alda-1 (20 μM/48 h) cultured in glucose free and galactose supplemented media. f ) Mitochondrial ROS measured by MitoSOX™ in control- and patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/36 h) cultured in glucose free and galactose supplemented media. g ) Cellular ATP levels measured using CellTiter-Glo Luminescent Cell Viability kit in control- and patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/48 h) cultured in glucose free and galactose supplemented media. h ) Mitochondrial ROS measured using MitoSOX™ in 2 control- and 2 AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM) 48 h after transfection with ALDH2*2. Each data point represents an average of 3 independent biological replicates from each subject. i ) Cellular ATP levels measured using CellTiter-Glo Luminescent Cell Viability kit in 2 control- and 2 AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM) 48 h after transfection with ALDH2*2. Each data point represents an average of 3 independent biological replicates from each subject. j ) Quantitation of basal respiration (OCR) as a measure of oxidative phosphorylation (OXPHOS) using Seahorse Extracellular Flux in one control- and one AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM) 48 h after transfection with ALDH2*2. k ) Quantitation of extracellular acidification rate (ECAR) as a measure of glycolytic dependence using Seahorse Extracellular Flux as in panel j. Data information: Mean, standard deviation, and p -values are shown. Results are presented as fold of control. n = 3 independent biological replicates; probability by one-way ANOVA (with Holm-Sidak post hoc test)
    Figure Legend Snippet: ALDH2*2 mutation is associated with increased oxidative stress in patient-derived fibroblasts with familial Alzheimer’s Disease (AD). a ) Genotyping of a Japanese AD patient-derived fibroblasts identifies heterozygous ALDH2*2/*1 mutation. ALDH2 protein expression in these cells was measured by immunoblotting three different culture passage numbers. b ) The levels of ALDH2 protein were determined in total lysates by immunoblotting of control (healthy subject; H)- and 2*2/*1 AD patient-derived fibroblasts. β-actin was used as loading control. c ) ALDH2 protein levels were quantified and represented as fold change of control. d ) Enzymatic activity of ALDH2 in lysates from ALDH2*2/*1 AD patient-derived fibroblasts relative to fibroblasts from control was measured over 5 min. e ) 4-HNE levels in control and AD patient-derived fibroblasts were measured using 4-HNE assay kit in the presence or absence of Alda-1 (20 μM/48 h) cultured in glucose free and galactose supplemented media. f ) Mitochondrial ROS measured by MitoSOX™ in control- and patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/36 h) cultured in glucose free and galactose supplemented media. g ) Cellular ATP levels measured using CellTiter-Glo Luminescent Cell Viability kit in control- and patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/48 h) cultured in glucose free and galactose supplemented media. h ) Mitochondrial ROS measured using MitoSOX™ in 2 control- and 2 AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM) 48 h after transfection with ALDH2*2. Each data point represents an average of 3 independent biological replicates from each subject. i ) Cellular ATP levels measured using CellTiter-Glo Luminescent Cell Viability kit in 2 control- and 2 AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM) 48 h after transfection with ALDH2*2. Each data point represents an average of 3 independent biological replicates from each subject. j ) Quantitation of basal respiration (OCR) as a measure of oxidative phosphorylation (OXPHOS) using Seahorse Extracellular Flux in one control- and one AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM) 48 h after transfection with ALDH2*2. k ) Quantitation of extracellular acidification rate (ECAR) as a measure of glycolytic dependence using Seahorse Extracellular Flux as in panel j. Data information: Mean, standard deviation, and p -values are shown. Results are presented as fold of control. n = 3 independent biological replicates; probability by one-way ANOVA (with Holm-Sidak post hoc test)

    Techniques Used: Mutagenesis, Derivative Assay, Expressing, Activity Assay, Cell Culture, Transfection, Quantitation Assay, Standard Deviation

    Ethanol increases metabolic dysfunction of Alzheimer’s disease (AD) patient-derived fibroblasts that is rescued by ALDH2 activation. a ) Measurement of mitochondrial ROS using MitoSOX™ in 4 control (healthy subject; H)- and 4 AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/48 h) and ethanol (50 mM). Each data point represents an average of 3 independent biological replicates from individual lines. b ) 4-HNE levels were measured using 4-HNE Assay Kit in control (healthy subject; H)- and AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/48 h) and ethanol (50 mM). Each data point represents an average of 3 independent biological replicates from individual lines. c ) Cellular ATP levels were analyzed using CellTiter-Glo Luminescent Cell Viability kit in control (healthy subject; H)- and AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/36 h) and ethanol (50 mM). Each data point represents an average of 3 independent biological replicates from individual lines. d ) Cellular ROS production was measured using 2,7 dichloro-fluorescein diacetate (DCFDA) in control (healthy subject; H) and AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/48 h) and ethanol (50 mM). Each data point represents an average of 3 independent biological replicates from individual lines. Data information: Mean, standard deviation, and p-values are shown. Results are presented as percent/fold of control. n = 3 independent biological replicates; probability by one-way ANOVA (with Holm-Sidak post hoc test)
    Figure Legend Snippet: Ethanol increases metabolic dysfunction of Alzheimer’s disease (AD) patient-derived fibroblasts that is rescued by ALDH2 activation. a ) Measurement of mitochondrial ROS using MitoSOX™ in 4 control (healthy subject; H)- and 4 AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/48 h) and ethanol (50 mM). Each data point represents an average of 3 independent biological replicates from individual lines. b ) 4-HNE levels were measured using 4-HNE Assay Kit in control (healthy subject; H)- and AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/48 h) and ethanol (50 mM). Each data point represents an average of 3 independent biological replicates from individual lines. c ) Cellular ATP levels were analyzed using CellTiter-Glo Luminescent Cell Viability kit in control (healthy subject; H)- and AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/36 h) and ethanol (50 mM). Each data point represents an average of 3 independent biological replicates from individual lines. d ) Cellular ROS production was measured using 2,7 dichloro-fluorescein diacetate (DCFDA) in control (healthy subject; H) and AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/48 h) and ethanol (50 mM). Each data point represents an average of 3 independent biological replicates from individual lines. Data information: Mean, standard deviation, and p-values are shown. Results are presented as percent/fold of control. n = 3 independent biological replicates; probability by one-way ANOVA (with Holm-Sidak post hoc test)

    Techniques Used: Derivative Assay, Activation Assay, Standard Deviation

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    Promega atp based celltiter glo luminescent cell viability kit
    Cultured primary neurons derived from ALDH2*2/*2 mice are more sensitive to ethanol-induced toxicity relative to primary neurons of WT mice. a ) LDH release a measure of cell death, was determined using LDH assay kit in primary neurons in the presence or absence of Alda-1 (20 μM/48 h) and ethanol (50 mM); Veh – Vehicle; A – Alda-1. b ) Cellular ROS production was determined using 2,7 dichloro- fluorescein diacetate (DCFDA) in primary neurons, treated as in a; Veh – Vehicle; A – Alda-1. c ) Measurement of cellular <t>ATP</t> levels using <t>CellTiter-Glo</t> Luminescent Cell Viability kit; Veh – Vehicle; A – Alda-1. d ) Quantitation of basal respiration (OCR) as a measure of oxidative phosphorylation (OXPHOS) using Seahorse Extracellular Flux in primary neurons treated as in a; Veh – Vehicle; A – Alda-1. e ) Quantitation of extracellular acidification rate (ECAR) as a measure of glycolytic dependence using Seahorse Extracellular Flux in primary neuron, treated as in a; Veh – Vehicle; A – Alda-1. f ) Levels of LC3B, TOM20, p53 and phosphorylation of JNK (Thr183/Tyr185) were determined in primary neurons, treated as in a, by immunoblotting. β-actin was used as loading control; Veh – Vehicle; A – Alda-1. Data information: Mean, standard deviation, and p-values are shown. Results are presented as percent/ fold of control. n = 3–4 independent biological replicates; probability by one-way ANOVA (with Holm-Sidak post hoc test)
    Atp Based Celltiter Glo Luminescent Cell Viability Kit, supplied by Promega, used in various techniques. Bioz Stars score: 92/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/atp based celltiter glo luminescent cell viability kit/product/Promega
    Average 92 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    atp based celltiter glo luminescent cell viability kit - by Bioz Stars, 2020-03
    92/100 stars
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    Cultured primary neurons derived from ALDH2*2/*2 mice are more sensitive to ethanol-induced toxicity relative to primary neurons of WT mice. a ) LDH release a measure of cell death, was determined using LDH assay kit in primary neurons in the presence or absence of Alda-1 (20 μM/48 h) and ethanol (50 mM); Veh – Vehicle; A – Alda-1. b ) Cellular ROS production was determined using 2,7 dichloro- fluorescein diacetate (DCFDA) in primary neurons, treated as in a; Veh – Vehicle; A – Alda-1. c ) Measurement of cellular ATP levels using CellTiter-Glo Luminescent Cell Viability kit; Veh – Vehicle; A – Alda-1. d ) Quantitation of basal respiration (OCR) as a measure of oxidative phosphorylation (OXPHOS) using Seahorse Extracellular Flux in primary neurons treated as in a; Veh – Vehicle; A – Alda-1. e ) Quantitation of extracellular acidification rate (ECAR) as a measure of glycolytic dependence using Seahorse Extracellular Flux in primary neuron, treated as in a; Veh – Vehicle; A – Alda-1. f ) Levels of LC3B, TOM20, p53 and phosphorylation of JNK (Thr183/Tyr185) were determined in primary neurons, treated as in a, by immunoblotting. β-actin was used as loading control; Veh – Vehicle; A – Alda-1. Data information: Mean, standard deviation, and p-values are shown. Results are presented as percent/ fold of control. n = 3–4 independent biological replicates; probability by one-way ANOVA (with Holm-Sidak post hoc test)

    Journal: Acta Neuropathologica Communications

    Article Title: Aldehyde dehydrogenase 2 activity and aldehydic load contribute to neuroinflammation and Alzheimer’s disease related pathology

    doi: 10.1186/s40478-019-0839-7

    Figure Lengend Snippet: Cultured primary neurons derived from ALDH2*2/*2 mice are more sensitive to ethanol-induced toxicity relative to primary neurons of WT mice. a ) LDH release a measure of cell death, was determined using LDH assay kit in primary neurons in the presence or absence of Alda-1 (20 μM/48 h) and ethanol (50 mM); Veh – Vehicle; A – Alda-1. b ) Cellular ROS production was determined using 2,7 dichloro- fluorescein diacetate (DCFDA) in primary neurons, treated as in a; Veh – Vehicle; A – Alda-1. c ) Measurement of cellular ATP levels using CellTiter-Glo Luminescent Cell Viability kit; Veh – Vehicle; A – Alda-1. d ) Quantitation of basal respiration (OCR) as a measure of oxidative phosphorylation (OXPHOS) using Seahorse Extracellular Flux in primary neurons treated as in a; Veh – Vehicle; A – Alda-1. e ) Quantitation of extracellular acidification rate (ECAR) as a measure of glycolytic dependence using Seahorse Extracellular Flux in primary neuron, treated as in a; Veh – Vehicle; A – Alda-1. f ) Levels of LC3B, TOM20, p53 and phosphorylation of JNK (Thr183/Tyr185) were determined in primary neurons, treated as in a, by immunoblotting. β-actin was used as loading control; Veh – Vehicle; A – Alda-1. Data information: Mean, standard deviation, and p-values are shown. Results are presented as percent/ fold of control. n = 3–4 independent biological replicates; probability by one-way ANOVA (with Holm-Sidak post hoc test)

    Article Snippet: ATP measurements Relative intracellular ATP levels were determined using ATP-based CellTiter-Glo Luminescent Cell Viability kit (Promega), which causes cell lysis and generates a luminescent signal proportional to the amount of ATP present.

    Techniques: Cell Culture, Derivative Assay, Mouse Assay, Lactate Dehydrogenase Assay, Quantitation Assay, Standard Deviation

    Cultured primary astrocyte derived from ALDH2*2/*2 mice are more activated in response to ethanol relative to primary astrocytes of WT mice. a ) Measurement of mitochondrial ROS using MitoSOX™ in primary astrocytes in the presence or absence of Alda-1 (20 μM/24 h; 50 mM Ethanol); Veh – Vehicle; A – Alda-1. b ) Heat map representation of qPCR analysis of genes associated with inflammation, apoptosis, autophagy and mitochondrial health; Veh – Vehicle; A – Alda-1. c ) Nitrite levels were determined in primary astrocytes using Griess reagent kit in the presence or absence of Alda-1 (20 μM/24 h; 50 mM Ethanol); Veh – Vehicle; A – Alda-1. d ) Measurement of cellular ATP levels using CellTiter-Glo Luminescent Cell Viability kit in primary astrocytes in the presence or absence of Alda-1 (20 μM/24 h; 50 mM Ethanol); Veh – Vehicle; A – Alda-1. e ) Levels of cellular COX-2 and interleukin-1β release at 6 h were determined by immunoblotting in primary astrocytes in the presence or absence of Alda-1 (20 μM; 50 mM Ethanol). β-actin was used as loading control; Veh – Vehicle; A – Alda-1. Data information: Mean, standard deviation, and p-values are shown. Results are presented as fold of control. n = 3–4 independent biological replicates; probability by one-way ANOVA (with Holm-Sidak post hoc test)

    Journal: Acta Neuropathologica Communications

    Article Title: Aldehyde dehydrogenase 2 activity and aldehydic load contribute to neuroinflammation and Alzheimer’s disease related pathology

    doi: 10.1186/s40478-019-0839-7

    Figure Lengend Snippet: Cultured primary astrocyte derived from ALDH2*2/*2 mice are more activated in response to ethanol relative to primary astrocytes of WT mice. a ) Measurement of mitochondrial ROS using MitoSOX™ in primary astrocytes in the presence or absence of Alda-1 (20 μM/24 h; 50 mM Ethanol); Veh – Vehicle; A – Alda-1. b ) Heat map representation of qPCR analysis of genes associated with inflammation, apoptosis, autophagy and mitochondrial health; Veh – Vehicle; A – Alda-1. c ) Nitrite levels were determined in primary astrocytes using Griess reagent kit in the presence or absence of Alda-1 (20 μM/24 h; 50 mM Ethanol); Veh – Vehicle; A – Alda-1. d ) Measurement of cellular ATP levels using CellTiter-Glo Luminescent Cell Viability kit in primary astrocytes in the presence or absence of Alda-1 (20 μM/24 h; 50 mM Ethanol); Veh – Vehicle; A – Alda-1. e ) Levels of cellular COX-2 and interleukin-1β release at 6 h were determined by immunoblotting in primary astrocytes in the presence or absence of Alda-1 (20 μM; 50 mM Ethanol). β-actin was used as loading control; Veh – Vehicle; A – Alda-1. Data information: Mean, standard deviation, and p-values are shown. Results are presented as fold of control. n = 3–4 independent biological replicates; probability by one-way ANOVA (with Holm-Sidak post hoc test)

    Article Snippet: ATP measurements Relative intracellular ATP levels were determined using ATP-based CellTiter-Glo Luminescent Cell Viability kit (Promega), which causes cell lysis and generates a luminescent signal proportional to the amount of ATP present.

    Techniques: Cell Culture, Derivative Assay, Mouse Assay, Real-time Polymerase Chain Reaction, Standard Deviation

    ALDH2*2 mutation is associated with increased oxidative stress in patient-derived fibroblasts with familial Alzheimer’s Disease (AD). a ) Genotyping of a Japanese AD patient-derived fibroblasts identifies heterozygous ALDH2*2/*1 mutation. ALDH2 protein expression in these cells was measured by immunoblotting three different culture passage numbers. b ) The levels of ALDH2 protein were determined in total lysates by immunoblotting of control (healthy subject; H)- and 2*2/*1 AD patient-derived fibroblasts. β-actin was used as loading control. c ) ALDH2 protein levels were quantified and represented as fold change of control. d ) Enzymatic activity of ALDH2 in lysates from ALDH2*2/*1 AD patient-derived fibroblasts relative to fibroblasts from control was measured over 5 min. e ) 4-HNE levels in control and AD patient-derived fibroblasts were measured using 4-HNE assay kit in the presence or absence of Alda-1 (20 μM/48 h) cultured in glucose free and galactose supplemented media. f ) Mitochondrial ROS measured by MitoSOX™ in control- and patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/36 h) cultured in glucose free and galactose supplemented media. g ) Cellular ATP levels measured using CellTiter-Glo Luminescent Cell Viability kit in control- and patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/48 h) cultured in glucose free and galactose supplemented media. h ) Mitochondrial ROS measured using MitoSOX™ in 2 control- and 2 AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM) 48 h after transfection with ALDH2*2. Each data point represents an average of 3 independent biological replicates from each subject. i ) Cellular ATP levels measured using CellTiter-Glo Luminescent Cell Viability kit in 2 control- and 2 AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM) 48 h after transfection with ALDH2*2. Each data point represents an average of 3 independent biological replicates from each subject. j ) Quantitation of basal respiration (OCR) as a measure of oxidative phosphorylation (OXPHOS) using Seahorse Extracellular Flux in one control- and one AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM) 48 h after transfection with ALDH2*2. k ) Quantitation of extracellular acidification rate (ECAR) as a measure of glycolytic dependence using Seahorse Extracellular Flux as in panel j. Data information: Mean, standard deviation, and p -values are shown. Results are presented as fold of control. n = 3 independent biological replicates; probability by one-way ANOVA (with Holm-Sidak post hoc test)

    Journal: Acta Neuropathologica Communications

    Article Title: Aldehyde dehydrogenase 2 activity and aldehydic load contribute to neuroinflammation and Alzheimer’s disease related pathology

    doi: 10.1186/s40478-019-0839-7

    Figure Lengend Snippet: ALDH2*2 mutation is associated with increased oxidative stress in patient-derived fibroblasts with familial Alzheimer’s Disease (AD). a ) Genotyping of a Japanese AD patient-derived fibroblasts identifies heterozygous ALDH2*2/*1 mutation. ALDH2 protein expression in these cells was measured by immunoblotting three different culture passage numbers. b ) The levels of ALDH2 protein were determined in total lysates by immunoblotting of control (healthy subject; H)- and 2*2/*1 AD patient-derived fibroblasts. β-actin was used as loading control. c ) ALDH2 protein levels were quantified and represented as fold change of control. d ) Enzymatic activity of ALDH2 in lysates from ALDH2*2/*1 AD patient-derived fibroblasts relative to fibroblasts from control was measured over 5 min. e ) 4-HNE levels in control and AD patient-derived fibroblasts were measured using 4-HNE assay kit in the presence or absence of Alda-1 (20 μM/48 h) cultured in glucose free and galactose supplemented media. f ) Mitochondrial ROS measured by MitoSOX™ in control- and patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/36 h) cultured in glucose free and galactose supplemented media. g ) Cellular ATP levels measured using CellTiter-Glo Luminescent Cell Viability kit in control- and patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/48 h) cultured in glucose free and galactose supplemented media. h ) Mitochondrial ROS measured using MitoSOX™ in 2 control- and 2 AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM) 48 h after transfection with ALDH2*2. Each data point represents an average of 3 independent biological replicates from each subject. i ) Cellular ATP levels measured using CellTiter-Glo Luminescent Cell Viability kit in 2 control- and 2 AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM) 48 h after transfection with ALDH2*2. Each data point represents an average of 3 independent biological replicates from each subject. j ) Quantitation of basal respiration (OCR) as a measure of oxidative phosphorylation (OXPHOS) using Seahorse Extracellular Flux in one control- and one AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM) 48 h after transfection with ALDH2*2. k ) Quantitation of extracellular acidification rate (ECAR) as a measure of glycolytic dependence using Seahorse Extracellular Flux as in panel j. Data information: Mean, standard deviation, and p -values are shown. Results are presented as fold of control. n = 3 independent biological replicates; probability by one-way ANOVA (with Holm-Sidak post hoc test)

    Article Snippet: ATP measurements Relative intracellular ATP levels were determined using ATP-based CellTiter-Glo Luminescent Cell Viability kit (Promega), which causes cell lysis and generates a luminescent signal proportional to the amount of ATP present.

    Techniques: Mutagenesis, Derivative Assay, Expressing, Activity Assay, Cell Culture, Transfection, Quantitation Assay, Standard Deviation

    Ethanol increases metabolic dysfunction of Alzheimer’s disease (AD) patient-derived fibroblasts that is rescued by ALDH2 activation. a ) Measurement of mitochondrial ROS using MitoSOX™ in 4 control (healthy subject; H)- and 4 AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/48 h) and ethanol (50 mM). Each data point represents an average of 3 independent biological replicates from individual lines. b ) 4-HNE levels were measured using 4-HNE Assay Kit in control (healthy subject; H)- and AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/48 h) and ethanol (50 mM). Each data point represents an average of 3 independent biological replicates from individual lines. c ) Cellular ATP levels were analyzed using CellTiter-Glo Luminescent Cell Viability kit in control (healthy subject; H)- and AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/36 h) and ethanol (50 mM). Each data point represents an average of 3 independent biological replicates from individual lines. d ) Cellular ROS production was measured using 2,7 dichloro-fluorescein diacetate (DCFDA) in control (healthy subject; H) and AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/48 h) and ethanol (50 mM). Each data point represents an average of 3 independent biological replicates from individual lines. Data information: Mean, standard deviation, and p-values are shown. Results are presented as percent/fold of control. n = 3 independent biological replicates; probability by one-way ANOVA (with Holm-Sidak post hoc test)

    Journal: Acta Neuropathologica Communications

    Article Title: Aldehyde dehydrogenase 2 activity and aldehydic load contribute to neuroinflammation and Alzheimer’s disease related pathology

    doi: 10.1186/s40478-019-0839-7

    Figure Lengend Snippet: Ethanol increases metabolic dysfunction of Alzheimer’s disease (AD) patient-derived fibroblasts that is rescued by ALDH2 activation. a ) Measurement of mitochondrial ROS using MitoSOX™ in 4 control (healthy subject; H)- and 4 AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/48 h) and ethanol (50 mM). Each data point represents an average of 3 independent biological replicates from individual lines. b ) 4-HNE levels were measured using 4-HNE Assay Kit in control (healthy subject; H)- and AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/48 h) and ethanol (50 mM). Each data point represents an average of 3 independent biological replicates from individual lines. c ) Cellular ATP levels were analyzed using CellTiter-Glo Luminescent Cell Viability kit in control (healthy subject; H)- and AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/36 h) and ethanol (50 mM). Each data point represents an average of 3 independent biological replicates from individual lines. d ) Cellular ROS production was measured using 2,7 dichloro-fluorescein diacetate (DCFDA) in control (healthy subject; H) and AD patient-derived fibroblasts in the presence or absence of Alda-1 (20 μM/48 h) and ethanol (50 mM). Each data point represents an average of 3 independent biological replicates from individual lines. Data information: Mean, standard deviation, and p-values are shown. Results are presented as percent/fold of control. n = 3 independent biological replicates; probability by one-way ANOVA (with Holm-Sidak post hoc test)

    Article Snippet: ATP measurements Relative intracellular ATP levels were determined using ATP-based CellTiter-Glo Luminescent Cell Viability kit (Promega), which causes cell lysis and generates a luminescent signal proportional to the amount of ATP present.

    Techniques: Derivative Assay, Activation Assay, Standard Deviation