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complex v activity assay kit  (Elabscience Biotechnology)


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    Elabscience Biotechnology complex v activity assay kit
    293 T cells were transfected with empty vector, wild-type Cend1, or the Cend1-G130P mutant for 48 h, followed by oxygen–glucose deprivation/reoxygenation (OGD/R) treatment. Cells were collected 24 h after reoxygenation for subsequent analyses. A Representative flow cytometric analysis of JC-1 staining showing the proportion of monomers and aggregates. B Quantification of JC-1 monomer proportion. N = 3. C Representative flow cytometric analysis of calcein–cobalt staining to assess mPTP opening. D Quantification of calcein fluorescence intensity. N = 3. E Relative NADH–CoQ reductase (complex I) activity measured using a mitochondrial complex I assay kit. N = 3. F Relative F₁F₀-ATP synthase (complex V) activity measured using a mitochondrial <t>complex</t> <t>V</t> assay kit. N = 3. G Intracellular ATP levels measured by ATP assay kit and normalized to protein content. N = 3. Data are presented as mean ± SEM. * P < 0.05; ** P < 0.01; ns, not significant.
    Complex V Activity Assay Kit, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mitochondrial+complex+f0f1+atpase/Cell+Mitochondrial+Complex+%E2%85%A4+(F0F1-ATPase%2FATP+Synthase)+Activity+Assay+Kit/pmc12902099-139-25-30
    Average 93 stars, based on 8 article reviews
    complex v activity assay kit - by Bioz Stars, 2026-08
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    Images

    1) Product Images from "Targeting Cend1-Atp5f1b interaction rescues mitochondrial dysfunction and ameliorates ischemic brain injury"

    Article Title: Targeting Cend1-Atp5f1b interaction rescues mitochondrial dysfunction and ameliorates ischemic brain injury

    Journal: Communications Biology

    doi: 10.1038/s42003-025-09419-4

    293 T cells were transfected with empty vector, wild-type Cend1, or the Cend1-G130P mutant for 48 h, followed by oxygen–glucose deprivation/reoxygenation (OGD/R) treatment. Cells were collected 24 h after reoxygenation for subsequent analyses. A Representative flow cytometric analysis of JC-1 staining showing the proportion of monomers and aggregates. B Quantification of JC-1 monomer proportion. N = 3. C Representative flow cytometric analysis of calcein–cobalt staining to assess mPTP opening. D Quantification of calcein fluorescence intensity. N = 3. E Relative NADH–CoQ reductase (complex I) activity measured using a mitochondrial complex I assay kit. N = 3. F Relative F₁F₀-ATP synthase (complex V) activity measured using a mitochondrial complex V assay kit. N = 3. G Intracellular ATP levels measured by ATP assay kit and normalized to protein content. N = 3. Data are presented as mean ± SEM. * P < 0.05; ** P < 0.01; ns, not significant.
    Figure Legend Snippet: 293 T cells were transfected with empty vector, wild-type Cend1, or the Cend1-G130P mutant for 48 h, followed by oxygen–glucose deprivation/reoxygenation (OGD/R) treatment. Cells were collected 24 h after reoxygenation for subsequent analyses. A Representative flow cytometric analysis of JC-1 staining showing the proportion of monomers and aggregates. B Quantification of JC-1 monomer proportion. N = 3. C Representative flow cytometric analysis of calcein–cobalt staining to assess mPTP opening. D Quantification of calcein fluorescence intensity. N = 3. E Relative NADH–CoQ reductase (complex I) activity measured using a mitochondrial complex I assay kit. N = 3. F Relative F₁F₀-ATP synthase (complex V) activity measured using a mitochondrial complex V assay kit. N = 3. G Intracellular ATP levels measured by ATP assay kit and normalized to protein content. N = 3. Data are presented as mean ± SEM. * P < 0.05; ** P < 0.01; ns, not significant.

    Techniques Used: Transfection, Plasmid Preparation, Mutagenesis, Staining, Fluorescence, Activity Assay, ATP Assay

    Cells were collected 24 h after reperfusion for subsequent assays. A Cells were stained with JC-1 at working concentration, and the ratio of JC-1 monomers to aggregates was analyzed by flow cytometry. B Quantification of JC-1 monomer proportion. N = 3. C Cells were stained with MPTP detection reagent at working concentration, and green fluorescence intensity was analyzed by flow cytometry. D Quantification of green fluorescence intensity reflecting mPTP opening. N = 3. E NADH–CoQ reductase activity was measured using a mitochondrial complex I activity assay kit according to the manufacturer’s instructions, and relative activity was quantified. N = 3. F F₁F₀-ATP synthase activity was measured using a complex V activity assay kit and quantified as relative activity. N = 3. G Intracellular ATP content was measured using a luminescence-based ATP assay kit and quantified relative to control. N = 3. Data are presented as mean ± SEM. * P < 0.05; ** P < 0.01; ns, not significant.
    Figure Legend Snippet: Cells were collected 24 h after reperfusion for subsequent assays. A Cells were stained with JC-1 at working concentration, and the ratio of JC-1 monomers to aggregates was analyzed by flow cytometry. B Quantification of JC-1 monomer proportion. N = 3. C Cells were stained with MPTP detection reagent at working concentration, and green fluorescence intensity was analyzed by flow cytometry. D Quantification of green fluorescence intensity reflecting mPTP opening. N = 3. E NADH–CoQ reductase activity was measured using a mitochondrial complex I activity assay kit according to the manufacturer’s instructions, and relative activity was quantified. N = 3. F F₁F₀-ATP synthase activity was measured using a complex V activity assay kit and quantified as relative activity. N = 3. G Intracellular ATP content was measured using a luminescence-based ATP assay kit and quantified relative to control. N = 3. Data are presented as mean ± SEM. * P < 0.05; ** P < 0.01; ns, not significant.

    Techniques Used: Staining, Concentration Assay, Flow Cytometry, Fluorescence, Activity Assay, ATP Assay, Control



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    293 T cells were transfected with empty vector, wild-type Cend1, or the Cend1-G130P mutant for 48 h, followed by oxygen–glucose deprivation/reoxygenation (OGD/R) treatment. Cells were collected 24 h after reoxygenation for subsequent analyses. A Representative flow cytometric analysis of JC-1 staining showing the proportion of monomers and aggregates. B Quantification of JC-1 monomer proportion. N = 3. C Representative flow cytometric analysis of calcein–cobalt staining to assess mPTP opening. D Quantification of calcein fluorescence intensity. N = 3. E Relative NADH–CoQ reductase (complex I) activity measured using a mitochondrial complex I assay kit. N = 3. F Relative F₁F₀-ATP synthase (complex V) activity measured using a mitochondrial <t>complex</t> <t>V</t> assay kit. N = 3. G Intracellular ATP levels measured by ATP assay kit and normalized to protein content. N = 3. Data are presented as mean ± SEM. * P < 0.05; ** P < 0.01; ns, not significant.
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    Image Search Results


    293 T cells were transfected with empty vector, wild-type Cend1, or the Cend1-G130P mutant for 48 h, followed by oxygen–glucose deprivation/reoxygenation (OGD/R) treatment. Cells were collected 24 h after reoxygenation for subsequent analyses. A Representative flow cytometric analysis of JC-1 staining showing the proportion of monomers and aggregates. B Quantification of JC-1 monomer proportion. N = 3. C Representative flow cytometric analysis of calcein–cobalt staining to assess mPTP opening. D Quantification of calcein fluorescence intensity. N = 3. E Relative NADH–CoQ reductase (complex I) activity measured using a mitochondrial complex I assay kit. N = 3. F Relative F₁F₀-ATP synthase (complex V) activity measured using a mitochondrial complex V assay kit. N = 3. G Intracellular ATP levels measured by ATP assay kit and normalized to protein content. N = 3. Data are presented as mean ± SEM. * P < 0.05; ** P < 0.01; ns, not significant.

    Journal: Communications Biology

    Article Title: Targeting Cend1-Atp5f1b interaction rescues mitochondrial dysfunction and ameliorates ischemic brain injury

    doi: 10.1038/s42003-025-09419-4

    Figure Lengend Snippet: 293 T cells were transfected with empty vector, wild-type Cend1, or the Cend1-G130P mutant for 48 h, followed by oxygen–glucose deprivation/reoxygenation (OGD/R) treatment. Cells were collected 24 h after reoxygenation for subsequent analyses. A Representative flow cytometric analysis of JC-1 staining showing the proportion of monomers and aggregates. B Quantification of JC-1 monomer proportion. N = 3. C Representative flow cytometric analysis of calcein–cobalt staining to assess mPTP opening. D Quantification of calcein fluorescence intensity. N = 3. E Relative NADH–CoQ reductase (complex I) activity measured using a mitochondrial complex I assay kit. N = 3. F Relative F₁F₀-ATP synthase (complex V) activity measured using a mitochondrial complex V assay kit. N = 3. G Intracellular ATP levels measured by ATP assay kit and normalized to protein content. N = 3. Data are presented as mean ± SEM. * P < 0.05; ** P < 0.01; ns, not significant.

    Article Snippet: Activities of mitochondrial complex I and V in 293 T cells were measured using the Cell Mitochondrial Complex I Activity Assay Kit (Elabscience, #E-BC-K834-M) and Complex V Activity Assay Kit (Elabscience, #E-BC-K838-M), respectively, according to the manufacturer’s instructions.

    Techniques: Transfection, Plasmid Preparation, Mutagenesis, Staining, Fluorescence, Activity Assay, ATP Assay

    Cells were collected 24 h after reperfusion for subsequent assays. A Cells were stained with JC-1 at working concentration, and the ratio of JC-1 monomers to aggregates was analyzed by flow cytometry. B Quantification of JC-1 monomer proportion. N = 3. C Cells were stained with MPTP detection reagent at working concentration, and green fluorescence intensity was analyzed by flow cytometry. D Quantification of green fluorescence intensity reflecting mPTP opening. N = 3. E NADH–CoQ reductase activity was measured using a mitochondrial complex I activity assay kit according to the manufacturer’s instructions, and relative activity was quantified. N = 3. F F₁F₀-ATP synthase activity was measured using a complex V activity assay kit and quantified as relative activity. N = 3. G Intracellular ATP content was measured using a luminescence-based ATP assay kit and quantified relative to control. N = 3. Data are presented as mean ± SEM. * P < 0.05; ** P < 0.01; ns, not significant.

    Journal: Communications Biology

    Article Title: Targeting Cend1-Atp5f1b interaction rescues mitochondrial dysfunction and ameliorates ischemic brain injury

    doi: 10.1038/s42003-025-09419-4

    Figure Lengend Snippet: Cells were collected 24 h after reperfusion for subsequent assays. A Cells were stained with JC-1 at working concentration, and the ratio of JC-1 monomers to aggregates was analyzed by flow cytometry. B Quantification of JC-1 monomer proportion. N = 3. C Cells were stained with MPTP detection reagent at working concentration, and green fluorescence intensity was analyzed by flow cytometry. D Quantification of green fluorescence intensity reflecting mPTP opening. N = 3. E NADH–CoQ reductase activity was measured using a mitochondrial complex I activity assay kit according to the manufacturer’s instructions, and relative activity was quantified. N = 3. F F₁F₀-ATP synthase activity was measured using a complex V activity assay kit and quantified as relative activity. N = 3. G Intracellular ATP content was measured using a luminescence-based ATP assay kit and quantified relative to control. N = 3. Data are presented as mean ± SEM. * P < 0.05; ** P < 0.01; ns, not significant.

    Article Snippet: Activities of mitochondrial complex I and V in 293 T cells were measured using the Cell Mitochondrial Complex I Activity Assay Kit (Elabscience, #E-BC-K834-M) and Complex V Activity Assay Kit (Elabscience, #E-BC-K838-M), respectively, according to the manufacturer’s instructions.

    Techniques: Staining, Concentration Assay, Flow Cytometry, Fluorescence, Activity Assay, ATP Assay, Control

    Astragaloside IV treatment of LPS-induced ER-autophagy in cardiomyocytes through DUSP1-PHB2 interaction. (A-B) Laser confocal detection of the endoplasmic reticulum. Scale bar, 25 μm (C-E) Detection of Complex I/III/V activity; (F) Detection of VDAC1 transcription level; (G) Detection of mPTP open level; (H-M) Detection of transcription levels of genes related to the mitochondrial unfolded protein response; (N) Detection of expression levels of pan-apoptosis related regulatory proteins; (O) Detection of endoplasmic reticulum autophagy expression level; Scale bar, 125 μm (P-S) Detection of transcription levels of pan-apoptosis related genes.Data are shown as mean ± SEM. Ten animals were used in each group and the dotes in each panel represent the average data of three replicates in each animal. *p < 0.05.

    Journal: Journal of Advanced Research

    Article Title: Astragaloside IV alleviates septic myocardial injury through DUSP1-Prohibitin 2 mediated mitochondrial quality control and ER-autophagy

    doi: 10.1016/j.jare.2024.10.030

    Figure Lengend Snippet: Astragaloside IV treatment of LPS-induced ER-autophagy in cardiomyocytes through DUSP1-PHB2 interaction. (A-B) Laser confocal detection of the endoplasmic reticulum. Scale bar, 25 μm (C-E) Detection of Complex I/III/V activity; (F) Detection of VDAC1 transcription level; (G) Detection of mPTP open level; (H-M) Detection of transcription levels of genes related to the mitochondrial unfolded protein response; (N) Detection of expression levels of pan-apoptosis related regulatory proteins; (O) Detection of endoplasmic reticulum autophagy expression level; Scale bar, 125 μm (P-S) Detection of transcription levels of pan-apoptosis related genes.Data are shown as mean ± SEM. Ten animals were used in each group and the dotes in each panel represent the average data of three replicates in each animal. *p < 0.05.

    Article Snippet: NO: Mouse MMP-9(Matrix Metalloproteinase 9) ELISA Kit E-EL-M3052, Elabscience, China);Mouse IL-10(Interleukin 10) ELISA Kit(E-EL-M0046, Elabscience, China);Mouse IL-17A(Interleukin 17A) ELISA Kit(E-EL-M0047, Elabscience, China);MDA(Malondialdehyde) ELISA Kit(E-EL-0060, Elabscience, China);A001-2-1 Superoxide Dismutase (SOD) Typing Test Kit(E-BC-K020-M, Elabscience, China);H545-1-1 Glutathione Peroxidase 4 (gpx4) Kit(E-BC-K096-S, Elabscience, China);Cell Mitochondrial Complex I (NADH-CoQ Reductase) Activity Assay Kit(E-BC-K834-M, Elabscience, China);Cell Mitochondrial Complex V (F0F1-ATPase/ATP Synthase) Activity Assay Kit (E-BC-K838-M, Elabscience, China);Cell Mitochondrial Complex III (Coenzyme Q-Cytochrome C Reductase) Activity Assay Kit(E-BC-K836-M, Elabscience, China);.

    Techniques: Activity Assay, Expressing