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opa1 polyclonal antibody  (Proteintech)


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    Structured Review

    Proteintech opa1 polyclonal antibody
    Nob ameliorated mitochondrial ultrastructure and function in D‐gal‐induced aging mice. (A) Mitochondrial ultrastructure, scale bar = 2 um or 500 μm, n = 3 mice/group. (B) Number of mitochondria. (C) Mitochondrial size. (D) Total cristae length per mitochondria area. (E) The activity of complex IV, n = 4 mice/group. (F) Total ATP production, n = 3. (G‐H) Western blot analysis of Mfn1, Mfn2, <t>OPA1,</t> Drp1 and β‐tubulin in D‐gal‐induced aging mice treated with vehicle and Nob, n = 3 mice/group. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
    Opa1 Polyclonal Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 285 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/opa1+polyclonal+antibody/OPA1+Antibody/pmc12784212-53-17-30
    Average 96 stars, based on 285 article reviews
    opa1 polyclonal antibody - by Bioz Stars, 2026-09
    96/100 stars

    Images

    1) Product Images from "Nobiletin Ameliorates Skeletal Muscle Performance in D‐Galactose‐Induced Aging Mice by Boosting Aerobic Metabolism"

    Article Title: Nobiletin Ameliorates Skeletal Muscle Performance in D‐Galactose‐Induced Aging Mice by Boosting Aerobic Metabolism

    Journal: Food Science & Nutrition

    doi: 10.1002/fsn3.71416

    Nob ameliorated mitochondrial ultrastructure and function in D‐gal‐induced aging mice. (A) Mitochondrial ultrastructure, scale bar = 2 um or 500 μm, n = 3 mice/group. (B) Number of mitochondria. (C) Mitochondrial size. (D) Total cristae length per mitochondria area. (E) The activity of complex IV, n = 4 mice/group. (F) Total ATP production, n = 3. (G‐H) Western blot analysis of Mfn1, Mfn2, OPA1, Drp1 and β‐tubulin in D‐gal‐induced aging mice treated with vehicle and Nob, n = 3 mice/group. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
    Figure Legend Snippet: Nob ameliorated mitochondrial ultrastructure and function in D‐gal‐induced aging mice. (A) Mitochondrial ultrastructure, scale bar = 2 um or 500 μm, n = 3 mice/group. (B) Number of mitochondria. (C) Mitochondrial size. (D) Total cristae length per mitochondria area. (E) The activity of complex IV, n = 4 mice/group. (F) Total ATP production, n = 3. (G‐H) Western blot analysis of Mfn1, Mfn2, OPA1, Drp1 and β‐tubulin in D‐gal‐induced aging mice treated with vehicle and Nob, n = 3 mice/group. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Techniques Used: Activity Assay, Western Blot

    Related Articles

    Pyrolysis Gas Chromatography:

    Article Title: Nobiletin Ameliorates Skeletal Muscle Performance in D‐Galactose‐Induced Aging Mice by Boosting Aerobic Metabolism
    Article Snippet: The mitochondrial respiratory chain complex IV activity assay kit ( bc 0945) was obtained from Beijing Solarbio Technology Co. Ltd. (Beijing, China). .. The PGC‐1α monoclonal antibody (66369‐1‐Ig), NRF2 Rabbit mAb (16396‐1‐AP), SIRT1 polyclonal antibody (13161‐1‐AP), MFN1 Polyclonal antibody (13798‐1‐AP), OPA1 Polyclonal antibody (27733‐1‐AP), and Beta Tubulin Polyclonal antibody (10094‐1‐AP) were purchased from Proteintech (Wuhan, China). .. The Mitofusin‐2 (D2D10) Rabbit mAb (9482) and DRP1 (4E11B11) Mouse mAb (14647) were obtained from Cell Signaling Technology.

    Article Title: JianPiYiShen formula prevents cisplatin-induced acute kidney injury in mice by improving necroptosis through MAPK pathway
    Article Snippet: Densitometric analysis of protein bands was conducted using Image-J (Bio-Rad, USA). .. The primary antibodies used in this experiment were as follows: Anti-NGAL antibody (1:1000, Lot No: ab41105) (Abcam, USA), Anti-SOD1 antibody (1:1000, Lot No: ab308181) (Abcam, USA), Anti-IL-10 antibody (1:1000, Lot No:ab34843) (Abcam, USA), Rabbit Anti-DRP1 (1:1000, Lot No: #8570s) (Cell Signaling Technology, USA), Rabbit Anti-Phospho-SAPK/JNK (1:1000, Lot No: #4668T) (Cell Signaling Technology, USA), Rabbit Anti-Phospho-RIP3 (1:1000, Lot No: #15828T) (Cell Signaling Technology, USA), Rabbit Anti-Phospho-MLKL (1:1000, Lot No: #37,333) (Cell Signaling Technology, USA), Anti-GAPDH (1:2000, Lot No: #2118) (Cell Signaling Technology, USA), Phospho-RIPK1 Monoclonal antibody (1:2000, Lot No:66854-1-Ig) (Proteintech, Wuhan, China), Phospho-ERK1/2 Polyclonal antibody (1:1000, Lot No:28733-1-AP) (Proteintech, Wuhan, China), ERK1/2 Polyclonal antibody (1:2000, Lot No: 11257-1-AP) (Proteintech, Wuhan, China), JNK Monoclonal antibody (1:3000, Lot No: 66210-1-Ig) (Proteintech, Wuhan, China), OPA1 Polyclonal antibody (1:1500, Lot No: 27733-1-AP) (Proteintech, Wuhan, China), MFF Polyclonal antibody (1:1000, Lot No: 17090-1-AP) (Proteintech, Wuhan, China), PGC-1α Monoclonal antibody (1:1000, Lot No:66369-1-Ig) (Proteintech, Wuhan, China), GAPDH Monoclonal antibody (1:5000, Lot No: 60004-1-Ig) (Proteintech, Wuhan, China), Anti-TNF-α (1:300, Lot No: sc-52,746) (Snata Cruz, USA), Anti-IL-6 (1:300, Lot No:sc-57,315) (Snata Cruz, USA), Anti-MCP-1 (1:300, Lot No: sc-52,701) (Snata Cruz, USA), and Mouse TIM-1/KIM-1/HAVCR Antibody (1:500, Lot No: AF1817) (R&D system, USA). .. MaxVision HRP-polymer anti-mouse/rabbit secondary antibodies (Lot No: KIT-5020; Maixin Biotech, Fujian, China) and Goat Anti-Rabbit IgG secondary antibody (Lot No: #L3012; Signalway, USA) were used in this experiment.

    Incubation:

    Article Title: Pioglitazone Alleviates β1-Adrenergic Receptor Antibody-Induced Atrial Fibrillation Susceptivity via Mitigation of PPAR-γ-Mediated Metabolic Inflexibility.
    Article Snippet: Xinjiang Key Laboratory of Cardiac Electrophysiology and Remodeling, The First Affiliated Hospital of Xinjiang Medical University, Urumqi 830011, China; Department of Pacing and Electrophysiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, China; Department of Cardiology, The Third People’s Hospital of Chengdu, Affiliated Hospital of Southwest Jiaotong University, Chengdu Cardiovascular Disease Research Institute, Chengdu 610014, Sichuan, China; Department of Cardiology, The First Affiliated Hospital of Shandong First Medical University and Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Jinan 250014, China; Medical Science and Technology Innovation Center, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan 250117, China



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    Nob ameliorated mitochondrial ultrastructure and function in D‐gal‐induced aging mice. (A) Mitochondrial ultrastructure, scale bar = 2 um or 500 μm, n = 3 mice/group. (B) Number of mitochondria. (C) Mitochondrial size. (D) Total cristae length per mitochondria area. (E) The activity of complex IV, n = 4 mice/group. (F) Total ATP production, n = 3. (G‐H) Western blot analysis of Mfn1, Mfn2, <t>OPA1,</t> Drp1 and β‐tubulin in D‐gal‐induced aging mice treated with vehicle and Nob, n = 3 mice/group. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
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    Nob ameliorated mitochondrial ultrastructure and function in D‐gal‐induced aging mice. (A) Mitochondrial ultrastructure, scale bar = 2 um or 500 μm, n = 3 mice/group. (B) Number of mitochondria. (C) Mitochondrial size. (D) Total cristae length per mitochondria area. (E) The activity of complex IV, n = 4 mice/group. (F) Total ATP production, n = 3. (G‐H) Western blot analysis of Mfn1, Mfn2, <t>OPA1,</t> Drp1 and β‐tubulin in D‐gal‐induced aging mice treated with vehicle and Nob, n = 3 mice/group. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
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    Image Search Results


    MSC-Exo treatment restored normalized mitochondrial dynamics by promoting OPA1 expression after ICH in vivo. A Representative images of mitochondrial morphology were captured using transmission electron microscopy, with scale bars:2 µm. B The mitochondria were categorized based on their length into three groups: <0.6 µm, 0.6–1.0 µm, and >1 µm ( n = 6 per group, one-way ANOVA). C Percentage of damaged mitochondria was calculated ( n = 6 per group, one-way ANOVA). D Representative western blots and quantitative results of OPA1, DRP1, and Mfn1/Mfn2 in the brain of mice. E–H The corresponding western blot data were statistically analyzed, and the results are displayed on the right side of the figures ( n = 6 per group, one-way ANOVA). Data are presented as mean ± SD, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001

    Journal: Molecular Neurobiology

    Article Title: Mesenchymal Stem Cell-derived Exosomes Alleviate Oxidative Stress and Brain Injuries Through Promoting OPA1 Mediated Mitochondrial Fusion After Intracerebral Hemorrhage

    doi: 10.1007/s12035-026-05703-4

    Figure Lengend Snippet: MSC-Exo treatment restored normalized mitochondrial dynamics by promoting OPA1 expression after ICH in vivo. A Representative images of mitochondrial morphology were captured using transmission electron microscopy, with scale bars:2 µm. B The mitochondria were categorized based on their length into three groups: <0.6 µm, 0.6–1.0 µm, and >1 µm ( n = 6 per group, one-way ANOVA). C Percentage of damaged mitochondria was calculated ( n = 6 per group, one-way ANOVA). D Representative western blots and quantitative results of OPA1, DRP1, and Mfn1/Mfn2 in the brain of mice. E–H The corresponding western blot data were statistically analyzed, and the results are displayed on the right side of the figures ( n = 6 per group, one-way ANOVA). Data are presented as mean ± SD, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001

    Article Snippet: After being immersed in 5% non-fat milk for 2 h, the membranes were treated with primary rabbit polyclonal antibodies against OPA1 (#80,471, CST, Danvers, MA, USA), DRP1 (#8570, CST, Danvers, MA, USA), Mitofusin-1 (13,798–1-AP, Proteintech, Rosemont, Illinois, USA), Mitofusin-2 (12,186–1-AP, Proteintech, Rosemont, Illinois, USA), CD81 (27,855–1-AP, Proteintech, Rosemont, Illinois, USA), TSG101 (28,283–1-AP, Proteintech, Rosemont, Illinois, USA), GM130 (PA5-95,727, Invitrogen, Carlsbad, CA, USA) overnight at 4 °C.

    Techniques: Expressing, In Vivo, Transmission Assay, Electron Microscopy, Western Blot

    Knockdown of Opa1 with siRNA blunted the protective effects of MSC-Exo in vitro. A Representative confocal microscopy images demonstrating mitochondrial morphology stained with MitoTracker are presented. B Relative aspect ratio statistical analysis was calculated ( n = 6 biological replicates, one-way ANOVA). C, D Representative images and quantitative appraisal of MitoSOX-stained mitochondria-associated superoxide generation are detailed ( n = 6 biological replicates, one-way ANOVA). E, F Effects of MSC-Exo treatment on MMP levels and NAD+/NADH levels ( n = 6 biological replicates, one-way ANOVA). Data are presented as mean ± SD, ** p < 0.01, *** p < 0.001, and **** p < 0.0001, ns, no statistical significance

    Journal: Molecular Neurobiology

    Article Title: Mesenchymal Stem Cell-derived Exosomes Alleviate Oxidative Stress and Brain Injuries Through Promoting OPA1 Mediated Mitochondrial Fusion After Intracerebral Hemorrhage

    doi: 10.1007/s12035-026-05703-4

    Figure Lengend Snippet: Knockdown of Opa1 with siRNA blunted the protective effects of MSC-Exo in vitro. A Representative confocal microscopy images demonstrating mitochondrial morphology stained with MitoTracker are presented. B Relative aspect ratio statistical analysis was calculated ( n = 6 biological replicates, one-way ANOVA). C, D Representative images and quantitative appraisal of MitoSOX-stained mitochondria-associated superoxide generation are detailed ( n = 6 biological replicates, one-way ANOVA). E, F Effects of MSC-Exo treatment on MMP levels and NAD+/NADH levels ( n = 6 biological replicates, one-way ANOVA). Data are presented as mean ± SD, ** p < 0.01, *** p < 0.001, and **** p < 0.0001, ns, no statistical significance

    Article Snippet: After being immersed in 5% non-fat milk for 2 h, the membranes were treated with primary rabbit polyclonal antibodies against OPA1 (#80,471, CST, Danvers, MA, USA), DRP1 (#8570, CST, Danvers, MA, USA), Mitofusin-1 (13,798–1-AP, Proteintech, Rosemont, Illinois, USA), Mitofusin-2 (12,186–1-AP, Proteintech, Rosemont, Illinois, USA), CD81 (27,855–1-AP, Proteintech, Rosemont, Illinois, USA), TSG101 (28,283–1-AP, Proteintech, Rosemont, Illinois, USA), GM130 (PA5-95,727, Invitrogen, Carlsbad, CA, USA) overnight at 4 °C.

    Techniques: Knockdown, In Vitro, Confocal Microscopy, Staining

    Neuron-specific Opa1 deletion blunted MSC-Exo protection of mitochondrial dynamics in vivo. A Representative images showcasing mitochondrial morphology as captured by transmission electron microscopy, scale bars:1 µm. B Mitochondrial fusion was assessed by Mitochondria length (<0.6 µm, 0.6–1.0 µm, >1 µm) ( n = 6 per group, two-way ANOVA). C Percentage of damaged mitochondria was calculated ( n = 6 per group, two-way ANOVA). D–G Effects of Opa1 knockout and MSC-Exo treatment on ATP levels, NAD+/NADH levels, and normalized complex I/II activity in the hippocampus ( n = 6 per group, two-way ANOVA). Data are presented as mean ± SD, ** p < 0.01 and *** p < 0.001, ns, no statistical significance

    Journal: Molecular Neurobiology

    Article Title: Mesenchymal Stem Cell-derived Exosomes Alleviate Oxidative Stress and Brain Injuries Through Promoting OPA1 Mediated Mitochondrial Fusion After Intracerebral Hemorrhage

    doi: 10.1007/s12035-026-05703-4

    Figure Lengend Snippet: Neuron-specific Opa1 deletion blunted MSC-Exo protection of mitochondrial dynamics in vivo. A Representative images showcasing mitochondrial morphology as captured by transmission electron microscopy, scale bars:1 µm. B Mitochondrial fusion was assessed by Mitochondria length (<0.6 µm, 0.6–1.0 µm, >1 µm) ( n = 6 per group, two-way ANOVA). C Percentage of damaged mitochondria was calculated ( n = 6 per group, two-way ANOVA). D–G Effects of Opa1 knockout and MSC-Exo treatment on ATP levels, NAD+/NADH levels, and normalized complex I/II activity in the hippocampus ( n = 6 per group, two-way ANOVA). Data are presented as mean ± SD, ** p < 0.01 and *** p < 0.001, ns, no statistical significance

    Article Snippet: After being immersed in 5% non-fat milk for 2 h, the membranes were treated with primary rabbit polyclonal antibodies against OPA1 (#80,471, CST, Danvers, MA, USA), DRP1 (#8570, CST, Danvers, MA, USA), Mitofusin-1 (13,798–1-AP, Proteintech, Rosemont, Illinois, USA), Mitofusin-2 (12,186–1-AP, Proteintech, Rosemont, Illinois, USA), CD81 (27,855–1-AP, Proteintech, Rosemont, Illinois, USA), TSG101 (28,283–1-AP, Proteintech, Rosemont, Illinois, USA), GM130 (PA5-95,727, Invitrogen, Carlsbad, CA, USA) overnight at 4 °C.

    Techniques: In Vivo, Transmission Assay, Electron Microscopy, Knock-Out, Activity Assay

    Neuron-specific Opa1 deletion blunted the protective effects of MSC-Exo treatment on oxidative stress and neurological outcomes after ICH. A, B Representative images depicting DHE staining and the quantitative assessment of DHE fluorescence intensity within the perilesional domain at 24 h post-intracerebral hemorrhage (ICH) are showcased, with a scale bar of 100 µm ( n = 6 per group, two-way ANOVA). C Effects of MSC-Exo treatment on MDA levels ( n = 6 per group, two-way ANOVA). D, F The reversal of the neuroprotective effects conferred by MSC-Exo in the context of neuronal-specific Opa1 conditional knockout is evaluated through behavioral assessments at various time points post-ICH, encompassing the Grid-walking test, Adhesive removal test, and Cylinder test ( n = 12 per group, two-way ANOVA). G The spatial learning and memory of subjects is further evaluated using the Morris water maze, portraying characteristic swim trajectories during the learning and memory phases of the assessment. H Mean swimming speed of mice in the MWM ( n = 12 per group, two-way ANOVA). I Spatial learning was evaluated through the measurement of escape latency in the Morris water maze from days 21 to 25 post-ICH ( n = 12 per group, two-way ANOVA). J, K Spatial memory is gauged by the duration spent in the target quadrant and the number of platform crossovers on day 26 following ICH ( n = 12 per group, two-way ANOVA). Data are presented as mean ± SD, ** p < 0.01, *** p < 0.001 and **** p < 0.0001

    Journal: Molecular Neurobiology

    Article Title: Mesenchymal Stem Cell-derived Exosomes Alleviate Oxidative Stress and Brain Injuries Through Promoting OPA1 Mediated Mitochondrial Fusion After Intracerebral Hemorrhage

    doi: 10.1007/s12035-026-05703-4

    Figure Lengend Snippet: Neuron-specific Opa1 deletion blunted the protective effects of MSC-Exo treatment on oxidative stress and neurological outcomes after ICH. A, B Representative images depicting DHE staining and the quantitative assessment of DHE fluorescence intensity within the perilesional domain at 24 h post-intracerebral hemorrhage (ICH) are showcased, with a scale bar of 100 µm ( n = 6 per group, two-way ANOVA). C Effects of MSC-Exo treatment on MDA levels ( n = 6 per group, two-way ANOVA). D, F The reversal of the neuroprotective effects conferred by MSC-Exo in the context of neuronal-specific Opa1 conditional knockout is evaluated through behavioral assessments at various time points post-ICH, encompassing the Grid-walking test, Adhesive removal test, and Cylinder test ( n = 12 per group, two-way ANOVA). G The spatial learning and memory of subjects is further evaluated using the Morris water maze, portraying characteristic swim trajectories during the learning and memory phases of the assessment. H Mean swimming speed of mice in the MWM ( n = 12 per group, two-way ANOVA). I Spatial learning was evaluated through the measurement of escape latency in the Morris water maze from days 21 to 25 post-ICH ( n = 12 per group, two-way ANOVA). J, K Spatial memory is gauged by the duration spent in the target quadrant and the number of platform crossovers on day 26 following ICH ( n = 12 per group, two-way ANOVA). Data are presented as mean ± SD, ** p < 0.01, *** p < 0.001 and **** p < 0.0001

    Article Snippet: After being immersed in 5% non-fat milk for 2 h, the membranes were treated with primary rabbit polyclonal antibodies against OPA1 (#80,471, CST, Danvers, MA, USA), DRP1 (#8570, CST, Danvers, MA, USA), Mitofusin-1 (13,798–1-AP, Proteintech, Rosemont, Illinois, USA), Mitofusin-2 (12,186–1-AP, Proteintech, Rosemont, Illinois, USA), CD81 (27,855–1-AP, Proteintech, Rosemont, Illinois, USA), TSG101 (28,283–1-AP, Proteintech, Rosemont, Illinois, USA), GM130 (PA5-95,727, Invitrogen, Carlsbad, CA, USA) overnight at 4 °C.

    Techniques: Staining, Fluorescence, Knock-Out, Adhesive

    Nob ameliorated mitochondrial ultrastructure and function in D‐gal‐induced aging mice. (A) Mitochondrial ultrastructure, scale bar = 2 um or 500 μm, n = 3 mice/group. (B) Number of mitochondria. (C) Mitochondrial size. (D) Total cristae length per mitochondria area. (E) The activity of complex IV, n = 4 mice/group. (F) Total ATP production, n = 3. (G‐H) Western blot analysis of Mfn1, Mfn2, OPA1, Drp1 and β‐tubulin in D‐gal‐induced aging mice treated with vehicle and Nob, n = 3 mice/group. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Journal: Food Science & Nutrition

    Article Title: Nobiletin Ameliorates Skeletal Muscle Performance in D‐Galactose‐Induced Aging Mice by Boosting Aerobic Metabolism

    doi: 10.1002/fsn3.71416

    Figure Lengend Snippet: Nob ameliorated mitochondrial ultrastructure and function in D‐gal‐induced aging mice. (A) Mitochondrial ultrastructure, scale bar = 2 um or 500 μm, n = 3 mice/group. (B) Number of mitochondria. (C) Mitochondrial size. (D) Total cristae length per mitochondria area. (E) The activity of complex IV, n = 4 mice/group. (F) Total ATP production, n = 3. (G‐H) Western blot analysis of Mfn1, Mfn2, OPA1, Drp1 and β‐tubulin in D‐gal‐induced aging mice treated with vehicle and Nob, n = 3 mice/group. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Article Snippet: The PGC‐1α monoclonal antibody (66369‐1‐Ig), NRF2 Rabbit mAb (16396‐1‐AP), SIRT1 polyclonal antibody (13161‐1‐AP), MFN1 Polyclonal antibody (13798‐1‐AP), OPA1 Polyclonal antibody (27733‐1‐AP), and Beta Tubulin Polyclonal antibody (10094‐1‐AP) were purchased from Proteintech (Wuhan, China).

    Techniques: Activity Assay, Western Blot

    Antibody description.

    Journal: PLOS ONE

    Article Title: Long-term consumption of hydrogen-rich water provides hepatoprotection by improving mitochondrial biology and quality control in chronically stressed mice

    doi: 10.1371/journal.pone.0317080

    Figure Lengend Snippet: Antibody description.

    Article Snippet: OPA1 , bs-11764R , Bioss , 1:1000.

    Techniques: