phosphor ampk rabbit mab  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphor ampk rabbit mab
    Phosphor Ampk Rabbit Mab, supplied by Cell Signaling Technology Inc, 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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    antibodies against phosphor ampk thr172  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc antibodies against phosphor ampk thr172
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    phosphor ampk thr172 cst  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphor ampk thr172 cst
    Phosphor Ampk Thr172 Cst, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rabbit monoclonal phosphor ampk  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit monoclonal phosphor ampk
    (A): FA oxidation was significantly increased in rat neonatal cardiac myocytes treated with 100 µM palmitic acid (PA). (B): On the other hand, glucose oxidation was significantly reduced in cardiac myocytes treated with PA (100 µM). (C): PA (50 to 100 µM) induced excessive FA oxidation was attenuated in cardiac myocytes transduced with a MOI of 20 of Ad-SCD1 (▪) in comparison with control cells transduced with Ad-LacZ (□). (D): PA (50 to 100 µM) -induced suppression of glucose oxidation recovered in cardiac myocytes transduced with Ad-SCD1 (▪) in comparison with control cells transduced with Ad-LacZ (□). BSA was used as a vehicle. Each sample was counted in a scintillation counter (cpm) and data are shown as the mean ± SD. **P<0.01 vs. Ad-LacZ in each PA concentration. (E); Phosphorylation levels of <t>AMPK</t> <t>and</t> <t>ACC</t> decreased in cardiac myocytes transduced with an MOI of 20 of Ad-SCD1 in comparison with control cells transduced with Ad-LacZ. Oligomycin (1 µM) was used as an AMPK and ACC activator.
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    1) Product Images from "Stearoyl-CoA Desaturase-1 (SCD1) Augments Saturated Fatty Acid-Induced Lipid Accumulation and Inhibits Apoptosis in Cardiac Myocytes"

    Article Title: Stearoyl-CoA Desaturase-1 (SCD1) Augments Saturated Fatty Acid-Induced Lipid Accumulation and Inhibits Apoptosis in Cardiac Myocytes

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0033283

    (A): FA oxidation was significantly increased in rat neonatal cardiac myocytes treated with 100 µM palmitic acid (PA). (B): On the other hand, glucose oxidation was significantly reduced in cardiac myocytes treated with PA (100 µM). (C): PA (50 to 100 µM) induced excessive FA oxidation was attenuated in cardiac myocytes transduced with a MOI of 20 of Ad-SCD1 (▪) in comparison with control cells transduced with Ad-LacZ (□). (D): PA (50 to 100 µM) -induced suppression of glucose oxidation recovered in cardiac myocytes transduced with Ad-SCD1 (▪) in comparison with control cells transduced with Ad-LacZ (□). BSA was used as a vehicle. Each sample was counted in a scintillation counter (cpm) and data are shown as the mean ± SD. **P<0.01 vs. Ad-LacZ in each PA concentration. (E); Phosphorylation levels of AMPK and ACC decreased in cardiac myocytes transduced with an MOI of 20 of Ad-SCD1 in comparison with control cells transduced with Ad-LacZ. Oligomycin (1 µM) was used as an AMPK and ACC activator.
    Figure Legend Snippet: (A): FA oxidation was significantly increased in rat neonatal cardiac myocytes treated with 100 µM palmitic acid (PA). (B): On the other hand, glucose oxidation was significantly reduced in cardiac myocytes treated with PA (100 µM). (C): PA (50 to 100 µM) induced excessive FA oxidation was attenuated in cardiac myocytes transduced with a MOI of 20 of Ad-SCD1 (▪) in comparison with control cells transduced with Ad-LacZ (□). (D): PA (50 to 100 µM) -induced suppression of glucose oxidation recovered in cardiac myocytes transduced with Ad-SCD1 (▪) in comparison with control cells transduced with Ad-LacZ (□). BSA was used as a vehicle. Each sample was counted in a scintillation counter (cpm) and data are shown as the mean ± SD. **P<0.01 vs. Ad-LacZ in each PA concentration. (E); Phosphorylation levels of AMPK and ACC decreased in cardiac myocytes transduced with an MOI of 20 of Ad-SCD1 in comparison with control cells transduced with Ad-LacZ. Oligomycin (1 µM) was used as an AMPK and ACC activator.

    Techniques Used: Transduction, Concentration Assay

    phosphor ampk antibody 2535t  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
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    Cell Signaling Technology Inc phosphor ampk antibody 2535t
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    phosphor ampk α  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphor ampk α
    (a–d) ARPE-19 cells were treated with 1 and 2.5 mM NaIO 3 for 48 h. (a) Mitochondrial membrane potential (MMP) in ARPE-19 cells was demonstrated by JC-1 staining, and the results were obtained by fluorescent microscopy. The red-to-green fluorescence intensity was used to quantitatively evaluate the mitochondrial potential; scale bar = 50 μ m ( n = 3). (b) Cellular ATP levels in ARPE-19 cells ( n = 5). (c) NAD + levels in ARPE-19 cells ( n = 3). (d) Expression of <t>AMPK</t> <t>α</t> and p-AMPK α proteins in ARPE-19 cells. (e) Immunofluorescence assay of mitochondrial outer membrane marker Tom20 was performed by confocal microscope. Cells were treated with 1 mM NaIO 3 for 48 hr; scale bar = 10 μ m ( n = 3) The mitochondrial branches length were measured by ImageJ. Data represent mean ± SD of at least three independent experiments, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, compared versus control.
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    1) Product Images from "Nicotinamide Mononucleotide Ameliorates Cellular Senescence and Inflammation Caused by Sodium Iodate in RPE"

    Article Title: Nicotinamide Mononucleotide Ameliorates Cellular Senescence and Inflammation Caused by Sodium Iodate in RPE

    Journal: Oxidative Medicine and Cellular Longevity

    doi: 10.1155/2022/5961123

    (a–d) ARPE-19 cells were treated with 1 and 2.5 mM NaIO 3 for 48 h. (a) Mitochondrial membrane potential (MMP) in ARPE-19 cells was demonstrated by JC-1 staining, and the results were obtained by fluorescent microscopy. The red-to-green fluorescence intensity was used to quantitatively evaluate the mitochondrial potential; scale bar = 50 μ m ( n = 3). (b) Cellular ATP levels in ARPE-19 cells ( n = 5). (c) NAD + levels in ARPE-19 cells ( n = 3). (d) Expression of AMPK α and p-AMPK α proteins in ARPE-19 cells. (e) Immunofluorescence assay of mitochondrial outer membrane marker Tom20 was performed by confocal microscope. Cells were treated with 1 mM NaIO 3 for 48 hr; scale bar = 10 μ m ( n = 3) The mitochondrial branches length were measured by ImageJ. Data represent mean ± SD of at least three independent experiments, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, compared versus control.
    Figure Legend Snippet: (a–d) ARPE-19 cells were treated with 1 and 2.5 mM NaIO 3 for 48 h. (a) Mitochondrial membrane potential (MMP) in ARPE-19 cells was demonstrated by JC-1 staining, and the results were obtained by fluorescent microscopy. The red-to-green fluorescence intensity was used to quantitatively evaluate the mitochondrial potential; scale bar = 50 μ m ( n = 3). (b) Cellular ATP levels in ARPE-19 cells ( n = 5). (c) NAD + levels in ARPE-19 cells ( n = 3). (d) Expression of AMPK α and p-AMPK α proteins in ARPE-19 cells. (e) Immunofluorescence assay of mitochondrial outer membrane marker Tom20 was performed by confocal microscope. Cells were treated with 1 mM NaIO 3 for 48 hr; scale bar = 10 μ m ( n = 3) The mitochondrial branches length were measured by ImageJ. Data represent mean ± SD of at least three independent experiments, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, compared versus control.

    Techniques Used: Staining, Microscopy, Fluorescence, Expressing, Immunofluorescence, Marker

    phosphor p ampk  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphor p ampk
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    anti phosphor ampk  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti phosphor ampk
    Anti Phosphor Ampk, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    phosphor ampk  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphor ampk
    Phosphor Ampk, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    phosphor ampk  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphor ampk
    Expression level of proteins involving in the glucolipid metabolic signaling pathway in the liver of mice: (a) representative immunoblot; (b–g) the expression levels of (b) <t>p-AMPK,</t> (c) SIRT1, (d) <t>PPAR</t> <t>α</t> , (e) PGC-1 α , (f) GLUT4, and (g) p-GSK-3 β proteins. Data are means ± SEM ( n = 6). ∗ p < 0.05 and ∗∗ p < 0.01 for the difference between sedentary and exercise regimes, as determined by two-way ANOVA and Tukey post hoc test. # p < 0.05 and ## p < 0.01 for the difference between WT and GCN2KO groups, as determined by two-way ANOVA and Tukey post hoc test.
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    1) Product Images from "GCN2 Deficiency Enhances Protective Effects of Exercise on Hepatic Steatosis"

    Article Title: GCN2 Deficiency Enhances Protective Effects of Exercise on Hepatic Steatosis

    Journal: BioMed Research International

    doi: 10.1155/2020/1454396

    Expression level of proteins involving in the glucolipid metabolic signaling pathway in the liver of mice: (a) representative immunoblot; (b–g) the expression levels of (b) p-AMPK, (c) SIRT1, (d) PPAR α , (e) PGC-1 α , (f) GLUT4, and (g) p-GSK-3 β proteins. Data are means ± SEM ( n = 6). ∗ p < 0.05 and ∗∗ p < 0.01 for the difference between sedentary and exercise regimes, as determined by two-way ANOVA and Tukey post hoc test. # p < 0.05 and ## p < 0.01 for the difference between WT and GCN2KO groups, as determined by two-way ANOVA and Tukey post hoc test.
    Figure Legend Snippet: Expression level of proteins involving in the glucolipid metabolic signaling pathway in the liver of mice: (a) representative immunoblot; (b–g) the expression levels of (b) p-AMPK, (c) SIRT1, (d) PPAR α , (e) PGC-1 α , (f) GLUT4, and (g) p-GSK-3 β proteins. Data are means ± SEM ( n = 6). ∗ p < 0.05 and ∗∗ p < 0.01 for the difference between sedentary and exercise regimes, as determined by two-way ANOVA and Tukey post hoc test. # p < 0.05 and ## p < 0.01 for the difference between WT and GCN2KO groups, as determined by two-way ANOVA and Tukey post hoc test.

    Techniques Used: Expressing, Western Blot

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    Cell Signaling Technology Inc phosphor ampk rabbit mab
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    (A): FA oxidation was significantly increased in rat neonatal cardiac myocytes treated with 100 µM palmitic acid (PA). (B): On the other hand, glucose oxidation was significantly reduced in cardiac myocytes treated with PA (100 µM). (C): PA (50 to 100 µM) induced excessive FA oxidation was attenuated in cardiac myocytes transduced with a MOI of 20 of Ad-SCD1 (▪) in comparison with control cells transduced with Ad-LacZ (□). (D): PA (50 to 100 µM) -induced suppression of glucose oxidation recovered in cardiac myocytes transduced with Ad-SCD1 (▪) in comparison with control cells transduced with Ad-LacZ (□). BSA was used as a vehicle. Each sample was counted in a scintillation counter (cpm) and data are shown as the mean ± SD. **P<0.01 vs. Ad-LacZ in each PA concentration. (E); Phosphorylation levels of <t>AMPK</t> <t>and</t> <t>ACC</t> decreased in cardiac myocytes transduced with an MOI of 20 of Ad-SCD1 in comparison with control cells transduced with Ad-LacZ. Oligomycin (1 µM) was used as an AMPK and ACC activator.
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    (A): FA oxidation was significantly increased in rat neonatal cardiac myocytes treated with 100 µM palmitic acid (PA). (B): On the other hand, glucose oxidation was significantly reduced in cardiac myocytes treated with PA (100 µM). (C): PA (50 to 100 µM) induced excessive FA oxidation was attenuated in cardiac myocytes transduced with a MOI of 20 of Ad-SCD1 (▪) in comparison with control cells transduced with Ad-LacZ (□). (D): PA (50 to 100 µM) -induced suppression of glucose oxidation recovered in cardiac myocytes transduced with Ad-SCD1 (▪) in comparison with control cells transduced with Ad-LacZ (□). BSA was used as a vehicle. Each sample was counted in a scintillation counter (cpm) and data are shown as the mean ± SD. **P<0.01 vs. Ad-LacZ in each PA concentration. (E); Phosphorylation levels of <t>AMPK</t> <t>and</t> <t>ACC</t> decreased in cardiac myocytes transduced with an MOI of 20 of Ad-SCD1 in comparison with control cells transduced with Ad-LacZ. Oligomycin (1 µM) was used as an AMPK and ACC activator.
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    (a–d) ARPE-19 cells were treated with 1 and 2.5 mM NaIO 3 for 48 h. (a) Mitochondrial membrane potential (MMP) in ARPE-19 cells was demonstrated by JC-1 staining, and the results were obtained by fluorescent microscopy. The red-to-green fluorescence intensity was used to quantitatively evaluate the mitochondrial potential; scale bar = 50 μ m ( n = 3). (b) Cellular ATP levels in ARPE-19 cells ( n = 5). (c) NAD + levels in ARPE-19 cells ( n = 3). (d) Expression of <t>AMPK</t> <t>α</t> and p-AMPK α proteins in ARPE-19 cells. (e) Immunofluorescence assay of mitochondrial outer membrane marker Tom20 was performed by confocal microscope. Cells were treated with 1 mM NaIO 3 for 48 hr; scale bar = 10 μ m ( n = 3) The mitochondrial branches length were measured by ImageJ. Data represent mean ± SD of at least three independent experiments, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, compared versus control.
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    (a–d) ARPE-19 cells were treated with 1 and 2.5 mM NaIO 3 for 48 h. (a) Mitochondrial membrane potential (MMP) in ARPE-19 cells was demonstrated by JC-1 staining, and the results were obtained by fluorescent microscopy. The red-to-green fluorescence intensity was used to quantitatively evaluate the mitochondrial potential; scale bar = 50 μ m ( n = 3). (b) Cellular ATP levels in ARPE-19 cells ( n = 5). (c) NAD + levels in ARPE-19 cells ( n = 3). (d) Expression of <t>AMPK</t> <t>α</t> and p-AMPK α proteins in ARPE-19 cells. (e) Immunofluorescence assay of mitochondrial outer membrane marker Tom20 was performed by confocal microscope. Cells were treated with 1 mM NaIO 3 for 48 hr; scale bar = 10 μ m ( n = 3) The mitochondrial branches length were measured by ImageJ. Data represent mean ± SD of at least three independent experiments, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, compared versus control.
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    (a–d) ARPE-19 cells were treated with 1 and 2.5 mM NaIO 3 for 48 h. (a) Mitochondrial membrane potential (MMP) in ARPE-19 cells was demonstrated by JC-1 staining, and the results were obtained by fluorescent microscopy. The red-to-green fluorescence intensity was used to quantitatively evaluate the mitochondrial potential; scale bar = 50 μ m ( n = 3). (b) Cellular ATP levels in ARPE-19 cells ( n = 5). (c) NAD + levels in ARPE-19 cells ( n = 3). (d) Expression of <t>AMPK</t> <t>α</t> and p-AMPK α proteins in ARPE-19 cells. (e) Immunofluorescence assay of mitochondrial outer membrane marker Tom20 was performed by confocal microscope. Cells were treated with 1 mM NaIO 3 for 48 hr; scale bar = 10 μ m ( n = 3) The mitochondrial branches length were measured by ImageJ. Data represent mean ± SD of at least three independent experiments, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, compared versus control.
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    (a–d) ARPE-19 cells were treated with 1 and 2.5 mM NaIO 3 for 48 h. (a) Mitochondrial membrane potential (MMP) in ARPE-19 cells was demonstrated by JC-1 staining, and the results were obtained by fluorescent microscopy. The red-to-green fluorescence intensity was used to quantitatively evaluate the mitochondrial potential; scale bar = 50 μ m ( n = 3). (b) Cellular ATP levels in ARPE-19 cells ( n = 5). (c) NAD + levels in ARPE-19 cells ( n = 3). (d) Expression of <t>AMPK</t> <t>α</t> and p-AMPK α proteins in ARPE-19 cells. (e) Immunofluorescence assay of mitochondrial outer membrane marker Tom20 was performed by confocal microscope. Cells were treated with 1 mM NaIO 3 for 48 hr; scale bar = 10 μ m ( n = 3) The mitochondrial branches length were measured by ImageJ. Data represent mean ± SD of at least three independent experiments, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, compared versus control.
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    (A): FA oxidation was significantly increased in rat neonatal cardiac myocytes treated with 100 µM palmitic acid (PA). (B): On the other hand, glucose oxidation was significantly reduced in cardiac myocytes treated with PA (100 µM). (C): PA (50 to 100 µM) induced excessive FA oxidation was attenuated in cardiac myocytes transduced with a MOI of 20 of Ad-SCD1 (▪) in comparison with control cells transduced with Ad-LacZ (□). (D): PA (50 to 100 µM) -induced suppression of glucose oxidation recovered in cardiac myocytes transduced with Ad-SCD1 (▪) in comparison with control cells transduced with Ad-LacZ (□). BSA was used as a vehicle. Each sample was counted in a scintillation counter (cpm) and data are shown as the mean ± SD. **P<0.01 vs. Ad-LacZ in each PA concentration. (E); Phosphorylation levels of AMPK and ACC decreased in cardiac myocytes transduced with an MOI of 20 of Ad-SCD1 in comparison with control cells transduced with Ad-LacZ. Oligomycin (1 µM) was used as an AMPK and ACC activator.

    Journal: PLoS ONE

    Article Title: Stearoyl-CoA Desaturase-1 (SCD1) Augments Saturated Fatty Acid-Induced Lipid Accumulation and Inhibits Apoptosis in Cardiac Myocytes

    doi: 10.1371/journal.pone.0033283

    Figure Lengend Snippet: (A): FA oxidation was significantly increased in rat neonatal cardiac myocytes treated with 100 µM palmitic acid (PA). (B): On the other hand, glucose oxidation was significantly reduced in cardiac myocytes treated with PA (100 µM). (C): PA (50 to 100 µM) induced excessive FA oxidation was attenuated in cardiac myocytes transduced with a MOI of 20 of Ad-SCD1 (▪) in comparison with control cells transduced with Ad-LacZ (□). (D): PA (50 to 100 µM) -induced suppression of glucose oxidation recovered in cardiac myocytes transduced with Ad-SCD1 (▪) in comparison with control cells transduced with Ad-LacZ (□). BSA was used as a vehicle. Each sample was counted in a scintillation counter (cpm) and data are shown as the mean ± SD. **P<0.01 vs. Ad-LacZ in each PA concentration. (E); Phosphorylation levels of AMPK and ACC decreased in cardiac myocytes transduced with an MOI of 20 of Ad-SCD1 in comparison with control cells transduced with Ad-LacZ. Oligomycin (1 µM) was used as an AMPK and ACC activator.

    Article Snippet: The mixture was rotated at 4°C for 15 min and centrifuged at 14000 rpm for 15 min. Western blot analysis was performed according to standard procedures using the following primary antibodies: rabbit monoclonal phosphor-AMPK, AMPK, phosphor-ACC, ACC, cleaved-caspase 3, caspase 3 mAb (Cell Signaling) and β-actin (Santa cruz biotechnology, CA, USA).

    Techniques: Transduction, Concentration Assay

    (a–d) ARPE-19 cells were treated with 1 and 2.5 mM NaIO 3 for 48 h. (a) Mitochondrial membrane potential (MMP) in ARPE-19 cells was demonstrated by JC-1 staining, and the results were obtained by fluorescent microscopy. The red-to-green fluorescence intensity was used to quantitatively evaluate the mitochondrial potential; scale bar = 50 μ m ( n = 3). (b) Cellular ATP levels in ARPE-19 cells ( n = 5). (c) NAD + levels in ARPE-19 cells ( n = 3). (d) Expression of AMPK α and p-AMPK α proteins in ARPE-19 cells. (e) Immunofluorescence assay of mitochondrial outer membrane marker Tom20 was performed by confocal microscope. Cells were treated with 1 mM NaIO 3 for 48 hr; scale bar = 10 μ m ( n = 3) The mitochondrial branches length were measured by ImageJ. Data represent mean ± SD of at least three independent experiments, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, compared versus control.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Nicotinamide Mononucleotide Ameliorates Cellular Senescence and Inflammation Caused by Sodium Iodate in RPE

    doi: 10.1155/2022/5961123

    Figure Lengend Snippet: (a–d) ARPE-19 cells were treated with 1 and 2.5 mM NaIO 3 for 48 h. (a) Mitochondrial membrane potential (MMP) in ARPE-19 cells was demonstrated by JC-1 staining, and the results were obtained by fluorescent microscopy. The red-to-green fluorescence intensity was used to quantitatively evaluate the mitochondrial potential; scale bar = 50 μ m ( n = 3). (b) Cellular ATP levels in ARPE-19 cells ( n = 5). (c) NAD + levels in ARPE-19 cells ( n = 3). (d) Expression of AMPK α and p-AMPK α proteins in ARPE-19 cells. (e) Immunofluorescence assay of mitochondrial outer membrane marker Tom20 was performed by confocal microscope. Cells were treated with 1 mM NaIO 3 for 48 hr; scale bar = 10 μ m ( n = 3) The mitochondrial branches length were measured by ImageJ. Data represent mean ± SD of at least three independent experiments, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, compared versus control.

    Article Snippet: The antibodies specific for p21 (#37543), Sirt1 (#2493), AMPK α (#5831), phosphor-AMPK α (Thr172, #2535), total-Akt (#4685), phosphor-Akt (Ser473, #4060), mTOR (#2983), and phosphor-mTOR (Ser2448, #5536), λ -H2AX (#2577) was purchased from Cell Signaling Technology (Beverly, MA, USA).

    Techniques: Staining, Microscopy, Fluorescence, Expressing, Immunofluorescence, Marker