antimycin a Search Results


antimycin a  (Thermo Fisher)
96
Thermo Fisher antimycin a
Metabolic profiling of wild-type (WT) and Trpv4 knockout (KO) macrophages via MitoStress Test. ( A , B ) Representative kinetic profiles of Oxygen Consumption Rate (OCR) and Extracellular Acidification Rate (ECAR). Real-time measurements of OCR (pmol/min) and ECAR (mpH/min) were performed under basal conditions and in response to the sequential injection of GSK2193874 (TRPV4 inhibitor, GSK21, 1 µM, individual data points are represented in the bar graphs by a triangle symbol) or vehicle (0.01% DMSO, individual data points are represented in the bar graphs by a dot symbol), followed by Oligomycin, FCCP, and Antimycin A/Rotenone. The untreated Trpv4 KO group is missing the values after the FCCP injection due to injection leakage. ( C ) No significant differences in basal OCR were observed between WT ( n = 9 technical replicates from 2 independent cultures) and Trpv4 KO ( n = 23 technical replicates from 3 independent cultures) cells across untreated or groups that received GKS21 injection ( n WT+GSK21 = 9 technical replicates from 2 independent cultures, n KO+GSK21 = 10 technical replicates from 3 independent cultures). ( D ) Acute treatment with GSK21, in WT cells, significantly increased non-mitochondrial oxygen consumption in both WT ( p = 0.0024) and Trpv4 KO ( p = 0.0461) cells compared to their respective vehicle-treated controls. ( E ) Calculated ATP-linked respiration showed a significant increase in Trpv4 KO cells following GSK21 administration ( p = 0.0031), while no significant change was observed in the WT cells. ( F ) No significant changes in proton leak were detected, indicating mitochondrial membrane integrity in all conditions. ( G ) Application of GSK21 significantly increased the glycolytic reserve of Trpv4 KO cells ( p = 0.0002) compared to their untreated counterparts. Data are represented as mean ± SEM. Statistical significance was determined by Two-way ANOVA, followed by Tukey’s post-hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001).
Antimycin A, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/antimycin+a/Antimycin+A/pmc12939844-156-50-71
Average 96 stars, based on 1 article reviews
antimycin a - by Bioz Stars, 2026-10
96/100 stars
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antimycin a  (Cell Signaling Technology Inc)
94
Cell Signaling Technology Inc antimycin a
Metabolic profiling of wild-type (WT) and Trpv4 knockout (KO) macrophages via MitoStress Test. ( A , B ) Representative kinetic profiles of Oxygen Consumption Rate (OCR) and Extracellular Acidification Rate (ECAR). Real-time measurements of OCR (pmol/min) and ECAR (mpH/min) were performed under basal conditions and in response to the sequential injection of GSK2193874 (TRPV4 inhibitor, GSK21, 1 µM, individual data points are represented in the bar graphs by a triangle symbol) or vehicle (0.01% DMSO, individual data points are represented in the bar graphs by a dot symbol), followed by Oligomycin, FCCP, and Antimycin A/Rotenone. The untreated Trpv4 KO group is missing the values after the FCCP injection due to injection leakage. ( C ) No significant differences in basal OCR were observed between WT ( n = 9 technical replicates from 2 independent cultures) and Trpv4 KO ( n = 23 technical replicates from 3 independent cultures) cells across untreated or groups that received GKS21 injection ( n WT+GSK21 = 9 technical replicates from 2 independent cultures, n KO+GSK21 = 10 technical replicates from 3 independent cultures). ( D ) Acute treatment with GSK21, in WT cells, significantly increased non-mitochondrial oxygen consumption in both WT ( p = 0.0024) and Trpv4 KO ( p = 0.0461) cells compared to their respective vehicle-treated controls. ( E ) Calculated ATP-linked respiration showed a significant increase in Trpv4 KO cells following GSK21 administration ( p = 0.0031), while no significant change was observed in the WT cells. ( F ) No significant changes in proton leak were detected, indicating mitochondrial membrane integrity in all conditions. ( G ) Application of GSK21 significantly increased the glycolytic reserve of Trpv4 KO cells ( p = 0.0002) compared to their untreated counterparts. Data are represented as mean ± SEM. Statistical significance was determined by Two-way ANOVA, followed by Tukey’s post-hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001).
Antimycin A, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/antimycin+a/Antimycin+A/pmc03501038-117-17-28
Average 94 stars, based on 1 article reviews
antimycin a - by Bioz Stars, 2026-10
94/100 stars
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antimycin a  (Santa Cruz Biotechnology)
94
Santa Cruz Biotechnology antimycin a
Metabolic profiling of wild-type (WT) and Trpv4 knockout (KO) macrophages via MitoStress Test. ( A , B ) Representative kinetic profiles of Oxygen Consumption Rate (OCR) and Extracellular Acidification Rate (ECAR). Real-time measurements of OCR (pmol/min) and ECAR (mpH/min) were performed under basal conditions and in response to the sequential injection of GSK2193874 (TRPV4 inhibitor, GSK21, 1 µM, individual data points are represented in the bar graphs by a triangle symbol) or vehicle (0.01% DMSO, individual data points are represented in the bar graphs by a dot symbol), followed by Oligomycin, FCCP, and Antimycin A/Rotenone. The untreated Trpv4 KO group is missing the values after the FCCP injection due to injection leakage. ( C ) No significant differences in basal OCR were observed between WT ( n = 9 technical replicates from 2 independent cultures) and Trpv4 KO ( n = 23 technical replicates from 3 independent cultures) cells across untreated or groups that received GKS21 injection ( n WT+GSK21 = 9 technical replicates from 2 independent cultures, n KO+GSK21 = 10 technical replicates from 3 independent cultures). ( D ) Acute treatment with GSK21, in WT cells, significantly increased non-mitochondrial oxygen consumption in both WT ( p = 0.0024) and Trpv4 KO ( p = 0.0461) cells compared to their respective vehicle-treated controls. ( E ) Calculated ATP-linked respiration showed a significant increase in Trpv4 KO cells following GSK21 administration ( p = 0.0031), while no significant change was observed in the WT cells. ( F ) No significant changes in proton leak were detected, indicating mitochondrial membrane integrity in all conditions. ( G ) Application of GSK21 significantly increased the glycolytic reserve of Trpv4 KO cells ( p = 0.0002) compared to their untreated counterparts. Data are represented as mean ± SEM. Statistical significance was determined by Two-way ANOVA, followed by Tukey’s post-hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001).
Antimycin A, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/antimycin+a/Antimycin+A/pmc12189359-37-47-66
Average 94 stars, based on 1 article reviews
antimycin a - by Bioz Stars, 2026-10
94/100 stars
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rotenone cn2  (LKT Laboratories)
86
LKT Laboratories rotenone cn2
Metabolic profiling of wild-type (WT) and Trpv4 knockout (KO) macrophages via MitoStress Test. ( A , B ) Representative kinetic profiles of Oxygen Consumption Rate (OCR) and Extracellular Acidification Rate (ECAR). Real-time measurements of OCR (pmol/min) and ECAR (mpH/min) were performed under basal conditions and in response to the sequential injection of GSK2193874 (TRPV4 inhibitor, GSK21, 1 µM, individual data points are represented in the bar graphs by a triangle symbol) or vehicle (0.01% DMSO, individual data points are represented in the bar graphs by a dot symbol), followed by Oligomycin, FCCP, and Antimycin A/Rotenone. The untreated Trpv4 KO group is missing the values after the FCCP injection due to injection leakage. ( C ) No significant differences in basal OCR were observed between WT ( n = 9 technical replicates from 2 independent cultures) and Trpv4 KO ( n = 23 technical replicates from 3 independent cultures) cells across untreated or groups that received GKS21 injection ( n WT+GSK21 = 9 technical replicates from 2 independent cultures, n KO+GSK21 = 10 technical replicates from 3 independent cultures). ( D ) Acute treatment with GSK21, in WT cells, significantly increased non-mitochondrial oxygen consumption in both WT ( p = 0.0024) and Trpv4 KO ( p = 0.0461) cells compared to their respective vehicle-treated controls. ( E ) Calculated ATP-linked respiration showed a significant increase in Trpv4 KO cells following GSK21 administration ( p = 0.0031), while no significant change was observed in the WT cells. ( F ) No significant changes in proton leak were detected, indicating mitochondrial membrane integrity in all conditions. ( G ) Application of GSK21 significantly increased the glycolytic reserve of Trpv4 KO cells ( p = 0.0002) compared to their untreated counterparts. Data are represented as mean ± SEM. Statistical significance was determined by Two-way ANOVA, followed by Tukey’s post-hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001).
Rotenone Cn2, supplied by LKT Laboratories, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 86 stars, based on 1 article reviews
rotenone cn2 - by Bioz Stars, 2026-10
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antimycin a  (Ayerst Laboratories)
90
Ayerst Laboratories antimycin a
Metabolic profiling of wild-type (WT) and Trpv4 knockout (KO) macrophages via MitoStress Test. ( A , B ) Representative kinetic profiles of Oxygen Consumption Rate (OCR) and Extracellular Acidification Rate (ECAR). Real-time measurements of OCR (pmol/min) and ECAR (mpH/min) were performed under basal conditions and in response to the sequential injection of GSK2193874 (TRPV4 inhibitor, GSK21, 1 µM, individual data points are represented in the bar graphs by a triangle symbol) or vehicle (0.01% DMSO, individual data points are represented in the bar graphs by a dot symbol), followed by Oligomycin, FCCP, and Antimycin A/Rotenone. The untreated Trpv4 KO group is missing the values after the FCCP injection due to injection leakage. ( C ) No significant differences in basal OCR were observed between WT ( n = 9 technical replicates from 2 independent cultures) and Trpv4 KO ( n = 23 technical replicates from 3 independent cultures) cells across untreated or groups that received GKS21 injection ( n WT+GSK21 = 9 technical replicates from 2 independent cultures, n KO+GSK21 = 10 technical replicates from 3 independent cultures). ( D ) Acute treatment with GSK21, in WT cells, significantly increased non-mitochondrial oxygen consumption in both WT ( p = 0.0024) and Trpv4 KO ( p = 0.0461) cells compared to their respective vehicle-treated controls. ( E ) Calculated ATP-linked respiration showed a significant increase in Trpv4 KO cells following GSK21 administration ( p = 0.0031), while no significant change was observed in the WT cells. ( F ) No significant changes in proton leak were detected, indicating mitochondrial membrane integrity in all conditions. ( G ) Application of GSK21 significantly increased the glycolytic reserve of Trpv4 KO cells ( p = 0.0002) compared to their untreated counterparts. Data are represented as mean ± SEM. Statistical significance was determined by Two-way ANOVA, followed by Tukey’s post-hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001).
Antimycin A, supplied by Ayerst Laboratories, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/antimycin+a/antimycin+a/pm04945811-9-38-10
Average 90 stars, based on 1 article reviews
antimycin a - by Bioz Stars, 2026-10
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oligomycin a  (CEM Corporation)
90
CEM Corporation oligomycin a
Metabolic profiling of wild-type (WT) and Trpv4 knockout (KO) macrophages via MitoStress Test. ( A , B ) Representative kinetic profiles of Oxygen Consumption Rate (OCR) and Extracellular Acidification Rate (ECAR). Real-time measurements of OCR (pmol/min) and ECAR (mpH/min) were performed under basal conditions and in response to the sequential injection of GSK2193874 (TRPV4 inhibitor, GSK21, 1 µM, individual data points are represented in the bar graphs by a triangle symbol) or vehicle (0.01% DMSO, individual data points are represented in the bar graphs by a dot symbol), followed by Oligomycin, FCCP, and Antimycin A/Rotenone. The untreated Trpv4 KO group is missing the values after the FCCP injection due to injection leakage. ( C ) No significant differences in basal OCR were observed between WT ( n = 9 technical replicates from 2 independent cultures) and Trpv4 KO ( n = 23 technical replicates from 3 independent cultures) cells across untreated or groups that received GKS21 injection ( n WT+GSK21 = 9 technical replicates from 2 independent cultures, n KO+GSK21 = 10 technical replicates from 3 independent cultures). ( D ) Acute treatment with GSK21, in WT cells, significantly increased non-mitochondrial oxygen consumption in both WT ( p = 0.0024) and Trpv4 KO ( p = 0.0461) cells compared to their respective vehicle-treated controls. ( E ) Calculated ATP-linked respiration showed a significant increase in Trpv4 KO cells following GSK21 administration ( p = 0.0031), while no significant change was observed in the WT cells. ( F ) No significant changes in proton leak were detected, indicating mitochondrial membrane integrity in all conditions. ( G ) Application of GSK21 significantly increased the glycolytic reserve of Trpv4 KO cells ( p = 0.0002) compared to their untreated counterparts. Data are represented as mean ± SEM. Statistical significance was determined by Two-way ANOVA, followed by Tukey’s post-hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001).
Oligomycin A, supplied by CEM Corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/antimycin+a/antimycin+a/pm29541451-223-42-61
Average 90 stars, based on 1 article reviews
oligomycin a - by Bioz Stars, 2026-10
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antimycin a  (Funakoshi ltd)
90
Funakoshi ltd antimycin a
Metabolic profiling of wild-type (WT) and Trpv4 knockout (KO) macrophages via MitoStress Test. ( A , B ) Representative kinetic profiles of Oxygen Consumption Rate (OCR) and Extracellular Acidification Rate (ECAR). Real-time measurements of OCR (pmol/min) and ECAR (mpH/min) were performed under basal conditions and in response to the sequential injection of GSK2193874 (TRPV4 inhibitor, GSK21, 1 µM, individual data points are represented in the bar graphs by a triangle symbol) or vehicle (0.01% DMSO, individual data points are represented in the bar graphs by a dot symbol), followed by Oligomycin, FCCP, and Antimycin A/Rotenone. The untreated Trpv4 KO group is missing the values after the FCCP injection due to injection leakage. ( C ) No significant differences in basal OCR were observed between WT ( n = 9 technical replicates from 2 independent cultures) and Trpv4 KO ( n = 23 technical replicates from 3 independent cultures) cells across untreated or groups that received GKS21 injection ( n WT+GSK21 = 9 technical replicates from 2 independent cultures, n KO+GSK21 = 10 technical replicates from 3 independent cultures). ( D ) Acute treatment with GSK21, in WT cells, significantly increased non-mitochondrial oxygen consumption in both WT ( p = 0.0024) and Trpv4 KO ( p = 0.0461) cells compared to their respective vehicle-treated controls. ( E ) Calculated ATP-linked respiration showed a significant increase in Trpv4 KO cells following GSK21 administration ( p = 0.0031), while no significant change was observed in the WT cells. ( F ) No significant changes in proton leak were detected, indicating mitochondrial membrane integrity in all conditions. ( G ) Application of GSK21 significantly increased the glycolytic reserve of Trpv4 KO cells ( p = 0.0002) compared to their untreated counterparts. Data are represented as mean ± SEM. Statistical significance was determined by Two-way ANOVA, followed by Tukey’s post-hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001).
Antimycin A, supplied by Funakoshi ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/antimycin+a/antimycin+a/pmc07848650__mmc1-204-0-4
Average 90 stars, based on 1 article reviews
antimycin a - by Bioz Stars, 2026-10
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antimycin a  (Federation of European Neuroscience Societies)
90
Federation of European Neuroscience Societies antimycin a
Metabolic profiling of wild-type (WT) and Trpv4 knockout (KO) macrophages via MitoStress Test. ( A , B ) Representative kinetic profiles of Oxygen Consumption Rate (OCR) and Extracellular Acidification Rate (ECAR). Real-time measurements of OCR (pmol/min) and ECAR (mpH/min) were performed under basal conditions and in response to the sequential injection of GSK2193874 (TRPV4 inhibitor, GSK21, 1 µM, individual data points are represented in the bar graphs by a triangle symbol) or vehicle (0.01% DMSO, individual data points are represented in the bar graphs by a dot symbol), followed by Oligomycin, FCCP, and Antimycin A/Rotenone. The untreated Trpv4 KO group is missing the values after the FCCP injection due to injection leakage. ( C ) No significant differences in basal OCR were observed between WT ( n = 9 technical replicates from 2 independent cultures) and Trpv4 KO ( n = 23 technical replicates from 3 independent cultures) cells across untreated or groups that received GKS21 injection ( n WT+GSK21 = 9 technical replicates from 2 independent cultures, n KO+GSK21 = 10 technical replicates from 3 independent cultures). ( D ) Acute treatment with GSK21, in WT cells, significantly increased non-mitochondrial oxygen consumption in both WT ( p = 0.0024) and Trpv4 KO ( p = 0.0461) cells compared to their respective vehicle-treated controls. ( E ) Calculated ATP-linked respiration showed a significant increase in Trpv4 KO cells following GSK21 administration ( p = 0.0031), while no significant change was observed in the WT cells. ( F ) No significant changes in proton leak were detected, indicating mitochondrial membrane integrity in all conditions. ( G ) Application of GSK21 significantly increased the glycolytic reserve of Trpv4 KO cells ( p = 0.0002) compared to their untreated counterparts. Data are represented as mean ± SEM. Statistical significance was determined by Two-way ANOVA, followed by Tukey’s post-hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001).
Antimycin A, supplied by Federation of European Neuroscience Societies, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
antimycin a - by Bioz Stars, 2026-10
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rotenone/antimycin a  (Merck KGaA)
90
Merck KGaA rotenone/antimycin a
Metabolic profiling of wild-type (WT) and Trpv4 knockout (KO) macrophages via MitoStress Test. ( A , B ) Representative kinetic profiles of Oxygen Consumption Rate (OCR) and Extracellular Acidification Rate (ECAR). Real-time measurements of OCR (pmol/min) and ECAR (mpH/min) were performed under basal conditions and in response to the sequential injection of GSK2193874 (TRPV4 inhibitor, GSK21, 1 µM, individual data points are represented in the bar graphs by a triangle symbol) or vehicle (0.01% DMSO, individual data points are represented in the bar graphs by a dot symbol), followed by Oligomycin, FCCP, and Antimycin A/Rotenone. The untreated Trpv4 KO group is missing the values after the FCCP injection due to injection leakage. ( C ) No significant differences in basal OCR were observed between WT ( n = 9 technical replicates from 2 independent cultures) and Trpv4 KO ( n = 23 technical replicates from 3 independent cultures) cells across untreated or groups that received GKS21 injection ( n WT+GSK21 = 9 technical replicates from 2 independent cultures, n KO+GSK21 = 10 technical replicates from 3 independent cultures). ( D ) Acute treatment with GSK21, in WT cells, significantly increased non-mitochondrial oxygen consumption in both WT ( p = 0.0024) and Trpv4 KO ( p = 0.0461) cells compared to their respective vehicle-treated controls. ( E ) Calculated ATP-linked respiration showed a significant increase in Trpv4 KO cells following GSK21 administration ( p = 0.0031), while no significant change was observed in the WT cells. ( F ) No significant changes in proton leak were detected, indicating mitochondrial membrane integrity in all conditions. ( G ) Application of GSK21 significantly increased the glycolytic reserve of Trpv4 KO cells ( p = 0.0002) compared to their untreated counterparts. Data are represented as mean ± SEM. Statistical significance was determined by Two-way ANOVA, followed by Tukey’s post-hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001).
Rotenone/Antimycin A, supplied by Merck KGaA, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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rotenone/antimycin a - by Bioz Stars, 2026-10
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antimycin a  (Merck KGaA)
90
Merck KGaA antimycin a
Metabolic profiling of wild-type (WT) and Trpv4 knockout (KO) macrophages via MitoStress Test. ( A , B ) Representative kinetic profiles of Oxygen Consumption Rate (OCR) and Extracellular Acidification Rate (ECAR). Real-time measurements of OCR (pmol/min) and ECAR (mpH/min) were performed under basal conditions and in response to the sequential injection of GSK2193874 (TRPV4 inhibitor, GSK21, 1 µM, individual data points are represented in the bar graphs by a triangle symbol) or vehicle (0.01% DMSO, individual data points are represented in the bar graphs by a dot symbol), followed by Oligomycin, FCCP, and Antimycin A/Rotenone. The untreated Trpv4 KO group is missing the values after the FCCP injection due to injection leakage. ( C ) No significant differences in basal OCR were observed between WT ( n = 9 technical replicates from 2 independent cultures) and Trpv4 KO ( n = 23 technical replicates from 3 independent cultures) cells across untreated or groups that received GKS21 injection ( n WT+GSK21 = 9 technical replicates from 2 independent cultures, n KO+GSK21 = 10 technical replicates from 3 independent cultures). ( D ) Acute treatment with GSK21, in WT cells, significantly increased non-mitochondrial oxygen consumption in both WT ( p = 0.0024) and Trpv4 KO ( p = 0.0461) cells compared to their respective vehicle-treated controls. ( E ) Calculated ATP-linked respiration showed a significant increase in Trpv4 KO cells following GSK21 administration ( p = 0.0031), while no significant change was observed in the WT cells. ( F ) No significant changes in proton leak were detected, indicating mitochondrial membrane integrity in all conditions. ( G ) Application of GSK21 significantly increased the glycolytic reserve of Trpv4 KO cells ( p = 0.0002) compared to their untreated counterparts. Data are represented as mean ± SEM. Statistical significance was determined by Two-way ANOVA, followed by Tukey’s post-hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001).
Antimycin A, supplied by Merck KGaA, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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rotenone/antimycin a  (Biomol GmbH)
90
Biomol GmbH rotenone/antimycin a
Metabolic profiling of wild-type (WT) and Trpv4 knockout (KO) macrophages via MitoStress Test. ( A , B ) Representative kinetic profiles of Oxygen Consumption Rate (OCR) and Extracellular Acidification Rate (ECAR). Real-time measurements of OCR (pmol/min) and ECAR (mpH/min) were performed under basal conditions and in response to the sequential injection of GSK2193874 (TRPV4 inhibitor, GSK21, 1 µM, individual data points are represented in the bar graphs by a triangle symbol) or vehicle (0.01% DMSO, individual data points are represented in the bar graphs by a dot symbol), followed by Oligomycin, FCCP, and Antimycin A/Rotenone. The untreated Trpv4 KO group is missing the values after the FCCP injection due to injection leakage. ( C ) No significant differences in basal OCR were observed between WT ( n = 9 technical replicates from 2 independent cultures) and Trpv4 KO ( n = 23 technical replicates from 3 independent cultures) cells across untreated or groups that received GKS21 injection ( n WT+GSK21 = 9 technical replicates from 2 independent cultures, n KO+GSK21 = 10 technical replicates from 3 independent cultures). ( D ) Acute treatment with GSK21, in WT cells, significantly increased non-mitochondrial oxygen consumption in both WT ( p = 0.0024) and Trpv4 KO ( p = 0.0461) cells compared to their respective vehicle-treated controls. ( E ) Calculated ATP-linked respiration showed a significant increase in Trpv4 KO cells following GSK21 administration ( p = 0.0031), while no significant change was observed in the WT cells. ( F ) No significant changes in proton leak were detected, indicating mitochondrial membrane integrity in all conditions. ( G ) Application of GSK21 significantly increased the glycolytic reserve of Trpv4 KO cells ( p = 0.0002) compared to their untreated counterparts. Data are represented as mean ± SEM. Statistical significance was determined by Two-way ANOVA, followed by Tukey’s post-hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001).
Rotenone/Antimycin A, supplied by Biomol GmbH, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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antimycin a/rotenone  (ChemScene llc)
90
ChemScene llc antimycin a/rotenone
Metabolic profiling of wild-type (WT) and Trpv4 knockout (KO) macrophages via MitoStress Test. ( A , B ) Representative kinetic profiles of Oxygen Consumption Rate (OCR) and Extracellular Acidification Rate (ECAR). Real-time measurements of OCR (pmol/min) and ECAR (mpH/min) were performed under basal conditions and in response to the sequential injection of GSK2193874 (TRPV4 inhibitor, GSK21, 1 µM, individual data points are represented in the bar graphs by a triangle symbol) or vehicle (0.01% DMSO, individual data points are represented in the bar graphs by a dot symbol), followed by Oligomycin, FCCP, and Antimycin A/Rotenone. The untreated Trpv4 KO group is missing the values after the FCCP injection due to injection leakage. ( C ) No significant differences in basal OCR were observed between WT ( n = 9 technical replicates from 2 independent cultures) and Trpv4 KO ( n = 23 technical replicates from 3 independent cultures) cells across untreated or groups that received GKS21 injection ( n WT+GSK21 = 9 technical replicates from 2 independent cultures, n KO+GSK21 = 10 technical replicates from 3 independent cultures). ( D ) Acute treatment with GSK21, in WT cells, significantly increased non-mitochondrial oxygen consumption in both WT ( p = 0.0024) and Trpv4 KO ( p = 0.0461) cells compared to their respective vehicle-treated controls. ( E ) Calculated ATP-linked respiration showed a significant increase in Trpv4 KO cells following GSK21 administration ( p = 0.0031), while no significant change was observed in the WT cells. ( F ) No significant changes in proton leak were detected, indicating mitochondrial membrane integrity in all conditions. ( G ) Application of GSK21 significantly increased the glycolytic reserve of Trpv4 KO cells ( p = 0.0002) compared to their untreated counterparts. Data are represented as mean ± SEM. Statistical significance was determined by Two-way ANOVA, followed by Tukey’s post-hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001).
Antimycin A/Rotenone, supplied by ChemScene llc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Metabolic profiling of wild-type (WT) and Trpv4 knockout (KO) macrophages via MitoStress Test. ( A , B ) Representative kinetic profiles of Oxygen Consumption Rate (OCR) and Extracellular Acidification Rate (ECAR). Real-time measurements of OCR (pmol/min) and ECAR (mpH/min) were performed under basal conditions and in response to the sequential injection of GSK2193874 (TRPV4 inhibitor, GSK21, 1 µM, individual data points are represented in the bar graphs by a triangle symbol) or vehicle (0.01% DMSO, individual data points are represented in the bar graphs by a dot symbol), followed by Oligomycin, FCCP, and Antimycin A/Rotenone. The untreated Trpv4 KO group is missing the values after the FCCP injection due to injection leakage. ( C ) No significant differences in basal OCR were observed between WT ( n = 9 technical replicates from 2 independent cultures) and Trpv4 KO ( n = 23 technical replicates from 3 independent cultures) cells across untreated or groups that received GKS21 injection ( n WT+GSK21 = 9 technical replicates from 2 independent cultures, n KO+GSK21 = 10 technical replicates from 3 independent cultures). ( D ) Acute treatment with GSK21, in WT cells, significantly increased non-mitochondrial oxygen consumption in both WT ( p = 0.0024) and Trpv4 KO ( p = 0.0461) cells compared to their respective vehicle-treated controls. ( E ) Calculated ATP-linked respiration showed a significant increase in Trpv4 KO cells following GSK21 administration ( p = 0.0031), while no significant change was observed in the WT cells. ( F ) No significant changes in proton leak were detected, indicating mitochondrial membrane integrity in all conditions. ( G ) Application of GSK21 significantly increased the glycolytic reserve of Trpv4 KO cells ( p = 0.0002) compared to their untreated counterparts. Data are represented as mean ± SEM. Statistical significance was determined by Two-way ANOVA, followed by Tukey’s post-hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001).

Journal: Cells

Article Title: TRPV4 Deficiency Shifts Mitochondrial Dynamics Toward a Fragmented Morphology in Primary Microglia

doi: 10.3390/cells15040341

Figure Lengend Snippet: Metabolic profiling of wild-type (WT) and Trpv4 knockout (KO) macrophages via MitoStress Test. ( A , B ) Representative kinetic profiles of Oxygen Consumption Rate (OCR) and Extracellular Acidification Rate (ECAR). Real-time measurements of OCR (pmol/min) and ECAR (mpH/min) were performed under basal conditions and in response to the sequential injection of GSK2193874 (TRPV4 inhibitor, GSK21, 1 µM, individual data points are represented in the bar graphs by a triangle symbol) or vehicle (0.01% DMSO, individual data points are represented in the bar graphs by a dot symbol), followed by Oligomycin, FCCP, and Antimycin A/Rotenone. The untreated Trpv4 KO group is missing the values after the FCCP injection due to injection leakage. ( C ) No significant differences in basal OCR were observed between WT ( n = 9 technical replicates from 2 independent cultures) and Trpv4 KO ( n = 23 technical replicates from 3 independent cultures) cells across untreated or groups that received GKS21 injection ( n WT+GSK21 = 9 technical replicates from 2 independent cultures, n KO+GSK21 = 10 technical replicates from 3 independent cultures). ( D ) Acute treatment with GSK21, in WT cells, significantly increased non-mitochondrial oxygen consumption in both WT ( p = 0.0024) and Trpv4 KO ( p = 0.0461) cells compared to their respective vehicle-treated controls. ( E ) Calculated ATP-linked respiration showed a significant increase in Trpv4 KO cells following GSK21 administration ( p = 0.0031), while no significant change was observed in the WT cells. ( F ) No significant changes in proton leak were detected, indicating mitochondrial membrane integrity in all conditions. ( G ) Application of GSK21 significantly increased the glycolytic reserve of Trpv4 KO cells ( p = 0.0002) compared to their untreated counterparts. Data are represented as mean ± SEM. Statistical significance was determined by Two-way ANOVA, followed by Tukey’s post-hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001).

Article Snippet: The sensor cartridge was loaded with compounds as follows: port A—either the TRPV4-specific inhibitor GSK2193874 (final concentration 1 μM) or vehicle control (final concentration 0.01% DMSO); port B—Oligomycin (ATP synthase inhibitor; final concentration 1.5 μM); port C—carbonyl cyanide-4 (phenylhydrazone) piperidine (FCCP; uncoupling agent; final concentration 1.5 μM); port D—combination of Antimycin A and Rotenone (mitochondrial complex III and I inhibitors; final concentrations 2.5 μM and 1.25 μM), co-injected with Hoechst 33342 (Thermo Fisher, Waltham, MA, USA) (final dilution 1:2500) to facilitate nuclear staining for cell normalization ( ).

Techniques: Knock-Out, Injection, Membrane