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Electron Transport Complex III

Electron Transport Complex III, also known as the cytochrome bc1 complex, is a crucial component of the mitochondrial electron transport chain.
This complex plays a central role in cellular respiration, catalyzing the oxidation of ubiquinol and the reduction of cytochrome c, thereby generating a proton gradient that drives ATP synthesis.
Reserach into the structure, function, and regulation of Electron Transport Complex III has implications for understanding energy metabolism, mitochondrial dysfunction, and various disease states.
PubCompare.ai's cutting-edge AI-driven protocol optimization can help navigaet the vast landscape of literature, pre-prints, and patents to uncover the best protocols and products for your Electron Transport Complex III reserach needs.

Most cited protocols related to «Electron Transport Complex III»

1
Mitochondrial Bioenergetics in Cardiomyocytes
Cited 25 times
An XF24 Analyzer (Seahorse Biosciences, North Billerica MA) was used to measure bioenergetic function in intact NRVM. The XF24 creates a transient, 7 μl chamber in specialized microplates that allows for oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) or proton production rate (PPR) to be monitored in real time [36 (link)]. For all bioenergetic measurements, the culture media was changed 1 h prior to the assay run to unbuffered Dulbecco’s Modified Eagle Medium (DMEM, pH 7.4) supplemented with 4 mM L-glutamine (Gibco, Carlsbad, CA). First, the optimum number of cells needed for these experiments was determined. NRVM were seeded to a density of 25,000, 50,000, or 75,000 cells/well. Oxygen consumption in these cells was linear with respect to cell number within this range (Fig. 1A), and a seeding density of 75,000 cells/well was chosen for the remainder of the experiments.
Next, an assay was developed to measure indices of mitochondrial function. Oligomycin, FCCP, and antimycin A were injected sequentially through ports in the Seahorse Flux Pak cartridges to final concentrations of 1 μg/ml, 1 μM, and 10 μM, respectively. This allowed determination of the basal level of oxygen consumption, the amount of oxygen consumption linked to ATP production, the level of non-ATP linked oxygen consumption (proton leak), the maximal respiration capacity, and the non-mitochondrial oxygen consumption. As shown in Fig. 1B, three basal OCR measurements were recorded prior to injection of oligomycin. After mixing and recording the oligomycin-sensitive OCR, FCCP was injected and another OCR measurement was recorded. The OCR measured after FCCP injection represents the maximal capacity that cells have to reduce oxygen under the experimental conditions. Finally, antimycin A was injected to inhibit the flux of electrons through complex III, and thus no oxygen is further consumed at cytochrome c oxidase. The remaining OCR determined after this treatment is primarily non-mitochondrial and could be due to cytosolic oxidase enzymes.
Hill B., Dranka B., Zou L., Chatham J, & Darley-Usmar V. (2009). Importance of the bioenergetic reserve capacity in response to cardiomyocyte stress induced by 4-hydroxynonenal. The Biochemical journal, 424(1), 99-107.
Publication 2009
Antimycin A Bioenergetics Biological Assay Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone Cardiac Arrest Cell Respiration Cells Cytosol Eagle Electrons Electron Transport Complex III Enzymes Glutamine Mitochondria Oligomycins Oxidase, Cytochrome-c Oxidases Oxygen Consumption PKN1 protein, human Protons Seahorses Training Programs Transients
2
Measuring Cellular Bioenergetics with Seahorse
Cited 19 times
Cellular bioenergetics of the isolated cells was determined using the extracellular flux analyzer (Seahorse Bioscience), which measures O2 and protons. This system allows for real-time, noninvasive measurements of O2 consumption rate (OCR) and proton production rate (PPR), which can be correlated to mitochondrial function/oxidative burst and glycolysis, respectively.43 (link) The injection ports attached to the wells allow for injection of inhibitors of mitochondrial respiratory chain or activators of the oxidative burst to determine the defects in individual cellular respiration pathways or enzymes. Pilot experiments for monocytes, neutrophils, platelets, and lymphocytes isolated from individual donors were performed to determine the optimal cell number required for accurate measurements of OCR and PPR. The optimum concentration of the inhibitors and activators to be used for the assessment of mitochondrial function and oxidative burst were determined by titrating the individual compounds in separate experiments against the cell number determined in the first set of experiments. First, the mean basal respiration is determined by taking 3–4 OCR measurements before the addition of the inhibitors or activators. ATP-linked OCR and proton leak were determined by injecting oligomycin at 0.5 μM (for monocytes, lymphocytes, and neutrophils) or 0.75 μM (for platelets). The fall in OCR following oligomycin injection is the rate of oxygen consumption that corresponds to ATP synthesis, and the oligomycin-insensitive rate is considered as proton leak across the inner mitochondrial membrane. FCCP, an uncoupler of the electron transport chain, was used at a concentration of 0.6 μM to determine the maximal respiration rate. This rate gives the theoretical maximum oxygen consumption that can take place at cytochrome c oxidase whether limited by availability of substrate or activity of the electron transport chain. The difference between the basal rate and this FCCP-stimulated rate is the reserve capacity of the mitochondrion, which is a measure of the maximal potential respiratory capacity the cell can utilize under conditions of stress and/or increased energetic demands. Antimycin A, an inhibitor of Complex III, was used to completely inhibit mitochondrial electron transport. The OCR determined after antimycin A injection is attributable to non-mitochondrial oxygen consumption. Mitochondrial basal respiration, proton leak, and the maximal respiration were calculated after correcting for the non-mitochondrial OCR for each assay. Cells were allowed to attach to the XF24 plate for 30–60 min before measurement of mitochondrial function. Under these conditions, viability was over 90% for all cell types and remained so over the time course of the assay. At the end of the assay period, cell lysates were collected, and OCR and PPR values normalized to the protein content in each well.
Chacko B.K., Kramer P.A., Ravi S., Johnson M.S., Hardy R.W., Ballinger S.W, & Darley-Usmar V.M. (2013). Methods for defining distinct bioenergetic profiles in platelets, lymphocytes, monocytes, and neutrophils, and the oxidative burst from human blood. Laboratory Investigation; a Journal of Technical Methods and Pathology, 93(6), 690-700.
Publication 2013
Anabolism Antimycin A Bioenergetics Biological Assay Biological Transport, Active Blood Platelets Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone Cardiac Arrest Cell Respiration Cells Donors Electrons Electron Transport Electron Transport Complex III Enzymes Glycolysis inhibitors Lymphocyte Mitochondria Mitochondrial Membrane, Inner Monocytes Neutrophil Oligomycins Oxidase, Cytochrome-c Oxygen Consumption Proteins Protons Respiratory Burst Respiratory Chain Respiratory Rate Seahorses Stress Disorders, Traumatic
3
Mitochondrial H2O2 Production Assay
Cited 17 times
Fill a cuvette with the incubation buffer (item 2, Subheading 2, see Note 13), add magnetic stirring bar, turn on the stirrer, and wait until the cuvette reaches the desired temperature (25–37°C). Add 4 U/ml of horseradish peroxidase, 10 μM Amplex Red Ultra, 40 U/ml superoxide dismutase (optional, see Note 12) and the same amount of mitochondria as used in step 3.3 to build the calibration curve. Record the fluorescence for ~150 s. Add respiratory substrates (see Note 6) and record H2O2 emission.
To illustrate a typical experimental protocol, Fig. 2 presents recordings of H2O2 production by isolated mouse brain mitochondria oxidizing NAD+-dependent substrates or succinate. The H2O2 generation is triggered by the addition of a respiratory substrate (succinate, Fig. 2a or pyruvate and malate, Fig. 2b, see Note 14). With NAD+-dependent substrates, H2O2 production was stimulated by rotenone, which inhibits NADH oxidation at Complex I (Fig. 2b). With succinate, rotenone inhibited H2O2 production indicating that it was fueled by reverse electron transfer from succinate to a site in Complex I (24 (link)). With either substrate, H2O2 production was stimulated by an inhibitor of Complex III (Antimycin A) (24 (link), 37 (link)).
, & Starkov A.A. (2010). Measurement of Mitochondrial ROS Production. Methods in molecular biology (Clifton, N.J.), 648, 245-255.
Publication 2010
Antimycin A Brain Buffers Electron Transport Electron Transport Complex III Fluorescence Horseradish Peroxidase malate Mitochondria Mus NADH NADH Dehydrogenase Complex 1 Peroxide, Hydrogen Pyruvate Respiratory Rate Rotenone Succinate Superoxide Dismutase
4
Mitochondrial Respiration and Glycolysis Profiling
Cited 14 times
We used the state-of-the-art Seahorse Extracellular Flux (XF) 96 Analyzer (Seahorse Bioscience, Inc, North Billerica, MA, USA), to measure the oxygen consumption rate (OCR), an indicator of mitochondrial respiration, and the extracellular acidification rate (ECAR), an indicator of glycolysis, in real-time in live intact LCLs.
Several measures of mitochondrial respiration, including basal respiration, ATP-linked respiration, proton leak respiration and reserve capacity, were derived by the sequential addition of pharmacological agents to the respiring cells, as diagramed in Figure 1. For each parameter, three repeated rates of oxygen consumption are made over an 18 minute period. First, baseline cellular oxygen consumption is measured, from which basal respiration is derived by subtracting non-mitochondrial respiration. Next oligomycin, an inhibitor of complex V, is added, and the resulting OCR is used to derive ATP-linked respiration (by subtracting the oligomycin rate from baseline cellular OCR) and proton leak respiration (by subtracting non-mitochondrial respiration from the oligomycin rate). Next carbonyl cyanide-p-trifluoromethoxyphenyl-hydrazon (FCCP), a protonophore, is added to collapse the inner membrane gradient, driving the ETC to function to its maximal rate, and maximal respiratory capacity is derived by subtracting non-mitochondrial respiration from the FCCP OCR. Lastly, antimycin A, a complex III inhibitor, and rotenone, a complex I inhibitor, are added to shut down ETC function, revealing the non-mitochondrial respiration. The mitochondrial reserve capacity is calculated by subtracting basal respiration from maximal respiratory capacity.
ECAR is primarily a measure of lactate production and can be equated to the glycolytic rate (i.e., glycolysis), and ECAR is measured simultaneously with OCR in the Seahorse assay. Basal ECAR refers to the ECAR measured before the injection of oligomycin. Glycolytic reserve capacity is calculated by subtracting the basal ECAR from the oligomycin-induced ECAR.
One hour prior to the assay, cells were seeded onto poly-D-lysine coated 96-well XF-PS plates at a density of 1.1×105 cells/well in DMEM XF assay media (unbuffered DMEM supplemented with 11 mM glucose, 2 mM L-glutamax, and 1 mM sodium pyruvate). Cells were plated with at least 4 replicate wells for each treatment group. Titrations were performed to determine the optimal concentrations of oligomycin (1.0 µM), FCCP (0.3 µM), antimycin A (0.3 µM) and rotenone (1.0 µM).
Rose S., Frye R.E., Slattery J., Wynne R., Tippett M., Pavliv O., Melnyk S, & James S.J. (2014). Oxidative Stress Induces Mitochondrial Dysfunction in a Subset of Autism Lymphoblastoid Cell Lines in a Well-Matched Case Control Cohort. PLoS ONE, 9(1), e85436.
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Publication 2014
Antimycin A Biological Assay Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone Cell Respiration Cells DNA Replication Electron Transport Complex III External Lateral Ligament Glucose Glycolysis Lactates Lysine mesoxalonitrile Mitochondria NADH Dehydrogenase Complex 1 Oligomycins oligomycin sensitivity-conferring protein Oxygen Consumption Poly A Protons Pyruvate Respiratory Rate Rotenone Seahorses Shock Sodium Tissue, Membrane Titrimetry
5
Bioenergetic Profiles of MCF-7 and MCF-10A Cells
Cited 9 times
The bioenergetic function of MCF-7 and MCF-10A cells in response to Mito-CP or 2-DG was determined using a Seahorse Bioscience XF24 Extracellular Flux Analyzer (Seahorse Bioscience). MCF-7 or MCF-10A cells were seeded in specialized V7 Seahorse tissue culture plates. One hour prior to the start of the experiment, cells were washed and changed to unbuffered assay medium adjusted to pH 7.4, final volume 675 µl (MEM-α for MCF-7, DMEM/F12 for MCF-10A). After establishing the baseline oxygen consumption rate (OCR) and extracellular acidification rate (ECAR), Mito-CP (1 µM) or 2-DG (5 mM) were administered through an automated pneumatic injection port of XF24. The changes in OCR and ECAR were monitored for 4 h. The resulting effects on OCR and ECAR are shown as a percentage of the baseline measurement for each treatment.
To determine the mitochondrial and glycolytic function of MCF-7 and MCF-10A cells in response to Mito-CP, Mito-Q, and 2-DG, we used the bioenergetic function assay previously described with several modifications (31 (link),32 (link)). After seeding and treatment as indicated, MCF-7 cells and MCF-10A cells were washed with complete media and either assayed immediately, or returned to a 37°C incubator for 36 or 60 h. The cells were then washed with unbuffered media as described above. Five baseline OCR and ECAR measurements were then taken before injection of oligomycin (1 µg/ml) to inhibit ATP synthase, FCCP (1–3 µM) to uncouple the mitochondria and yield maximal OCR, and antimycin A (10 µM) to prevent mitochondrial oxygen consumption through inhibition of Complex III. From these measurements, indices of mitochondrial function were determined as previously described (31 (link),32 (link)).
Cheng G., Zielonka J., Dranka B.P., McAllister D., Mackinnon AC J.r., Joseph J, & Kalyanaraman B. (2012). Mitochondria targeted drugs synergize with 2-deoxyglucose to trigger breast cancer cell death. Cancer research, 72(10), 2634-2644.
Publication 2012
Antimycin A Bioenergetics Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone Cardiac Arrest Cells Electron Transport Complex III Glycolysis MCF-7 Cells mito-carboxy proxyl Mitochondria MitoQ Nitric Oxide Synthase Oligomycins Oxygen Consumption Psychological Inhibition Seahorses Tissues

Most recents protocols related to «Electron Transport Complex III»

1
Water-Forming NADH Oxidases Restore Proliferation
Not available on PMC !

Example 8

GiNOX, a water-forming NADH oxidase derived from Giardia intestinalis, and mitoGiNOX are capable of restoring the proliferation of mammalian cells cultured in pyruvate-depleted media and in the presence of antimycin, a complex III inhibitor. HeLa Tet3G cells cultured in the presence of varying concentrations of pyruvate demonstrated a diminished pyruvate-dependency in the presence of antimycin when GiNOX and mitoGiNOX were expressed in these cells (FIG. 13). Notably, both GiNOX and mitoGiNOX were capable of alleviating the pyruvate auxotrophy, which further illustrates that cytosolic water-forming NADH oxidases can ameliorate the effects of a defective respiratory chain, as these enzymes need not be targeted to the mitochondria in order to restore redox balance.

US11866736B2. Protein prostheses for mitochondrial diseases or conditions (2024-01-09). The General Hospital Corporation [US]. Inventors: Vamsi Mootha [US], Denis Titov [US], Valentin Cracan [US], Zenon Grabarek [US].
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Patent 2024
antimycin Antimycin A Cell Proliferation Cells Culture Media Cytosol Electron Transport Complex III Enzymes Eukaryotic Cells Giardia lamblia HeLa Cells Mammals Mitochondria NADH Oxidation-Reduction Pyruvate Respiratory Chain Water-Splitting Enzyme of Photosynthesis
2
Seahorse XFp Assay for T-cell Metabolic Profiling
On the day prior to the assay, the Agilent Seahorse XFp Sensor Cartridge with XF Calibrant was hydrated in a non-CO2 37°C incubator overnight. Isolated T cells co-treated with eicosenoate were stimulated with ImmunoCult Human CD3/CD28 T-cell Activator (StemCell Technologies, Vancouver, Canada) for 24 h. On the day of the assay, cells were resuspended in warmed assay medium to the desired concentration (5×105 cells in 50μl/well) before seeding them onto the CellTak-coated Seahorse Cell Culture Miniplate (wells A and H were used as background correction wells). Then, cells were centrifuged at 350×g for 5 mins, and 130μl assay medium was added to each well for a final volume of 180μl. Finally, the Miniplate was transferred to a non-CO2 37°C incubator for 20 mins to ensure that the cells were entirely stable. Oxygen consumption rate (OCR) was measured without adding any drug (basal respiration), followed by measurement of OCR changes upon subsequent addition of 1.5 μM ATP synthase inhibitor oligomycin and 1 μM carbonyl cyanide-4 (trifluoromethoxy), and phenylhydrazone (FCCP). Finally, 0.5 μM rotenone and 0.5 μM antimycin A were injected to completely inhibit mitochondrial respiration by blocking complex I and complex III. Basal respiration, maximal respiration, and spare respiration were analyzed using an XFp Cell Mito Stress Tests Kit on an Agilent Seahorse XF HS Mini instrument, according to the corresponding operation protocol.
Li S.Y., Yin L.B., Ding H.B., Liu M., Lv J.N., Li J.Q., Wang J., Tang T., Fu Y.J., Jiang Y.J., Zhang Z.N, & Shang H. (2023). Altered lipid metabolites accelerate early dysfunction of T cells in HIV-infected rapid progressors by impairing mitochondrial function. Frontiers in Immunology, 14, 1106881.
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Publication 2023
Antimycin A Biological Assay Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone Cardiac Arrest Cell Culture Techniques Cell Respiration Cells Electron Transport Complex III Exercise Tests Homo sapiens mesoxalonitrile Mitomycin NADH Dehydrogenase Complex 1 NOS1 protein, human Oligomycins Oxygen Consumption Pharmaceutical Preparations phenylhydrazone Rotenone Seahorses Stem Cells T-Lymphocyte
3
Measuring Platelet and PBMC Oxygen Consumption
Platelet and PBMCs isolation and oxygen consumption rate (OCR) analyses were performed as previously described [7 (link)]. Briefly, blood samples were obtained in BD Vacutainer tubes containing EDTA after an overnight fast. Platelets were isolated by centrifugation, while PBMCs were isolated by density gradient centrifugation using Lymphoprep™ (Stemcell Technologies), according to the manufacturer’s instructions. Platelet and PBMCs concentrations were determined using the automated cell counter Z1 Coulter Particle Counter (Beckman).
Oxygen consumption rate (OCR) analyses were performed in a Seahorse XFe24 extracellular flux analyzer (Agilent). Purified platelets were seeded (2.5 × 107 cells/well) in 100 µl of Seahorse medium (8.3 g/L DMEM, 1.85 g/L NaCl, 5 mM glucose, 1 mM pyruvate, 2 mM glutamine, 5 mM HEPES, pH 7.4) on XFe24 V7 cell culture plates (Agilent), and the plates centrifuged at 300 g for 10 min to attach the platelets to the bottom of the plate. PBMCs were seeded (4 × 105 cells/well in 100 µl of Seahorse medium) on poly-D-lysine coated XFe24 V7cell culture plates and incubated for 30 min at 37 °C to allow the adhesion to the plate. Seahorse medium (500 µl) was added to each well; plates were kept at 37 °C for approximately 1 h and loaded into the instrument.
Oxygen consumption rate was measured before and after the sequential addition of 2.5 µM oligomycin (ATP synthase inhibitor), cyanide p- (trifluoro-methoxy) phenyl-hydrazone (FCCP, uncoupler 0.5–3 µM) and 2.5/2.5 µM antimycin A/rotenone (complex III and I inhibitors, respectively). The non-mitochondrial oxygen consumption rate (obtained after the addition of antimycin A/rotenone) was subtracted from all measurements. Respiratory parameters were obtained as follows: basal (baseline OCR); ATP-independent (OCR resistant to the addition of oligomycin, proton leak); ATP-dependent (basal—ATP-independent); maximum (OCR obtained after the addition of FCCP); spare respiratory capacity (maximum—basal) [17 (link)]. Respiration was normalized considering cell number.
Raggio V., Graña M., Winiarski E., Mansilla S., Simoes C., Rodríguez S., Brandes M., Tapié A., Rodríguez L., Cibils L., Alonso M., Martínez J., Fernández-Calero T., Domínguez F., Mezquida M.R., Castro L., Cerisola A., Naya H., Cassina A., Quijano C, & Spangenberg L. (2023). Computational and mitochondrial functional studies of novel compound heterozygous variants in SPATA5 gene support a causal link with epileptogenic encephalopathy. Human Genomics, 17, 14.
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Publication 2023
Antimycin A Blood Blood Platelets Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone Cell Culture Techniques Cell Respiration Cells Centrifugation Centrifugation, Density Gradient Cyanides Edetic Acid Electron Transport Complex III Glucose Glutamine HEPES Hydrazones inhibitors isolation lymphoprep Lysine Mitochondria Nitric Oxide Synthase Oligomycins Oxygen Consumption Poly A Protons Pyruvate Respiratory Rate Rotenone Seahorses Sodium Chloride Stem Cells
4
Mitochondrial Respiratory Complex Assay
Skeletal muscle mitochondria were resuspended in 10 mM Tris-HCL pH 7.6. The spectrophotometric activity of complex I (CI), complex II (CII), complex III (CIII), and complex IV (CIV), as well as citrate synthase (CS), was measured as described in Brischigliaro et al. [34 (link)].
Chemello F., Pozzobon M., Tsansizi L.I., Varanita T., Quintana-Cabrera R., Bonesso D., Piccoli M., Lanfranchi G., Giacomello M., Scorrano L, & Bean C. (2023). Dysfunctional mitochondria accumulate in a skeletal muscle knockout model of Smn1, the causal gene of spinal muscular atrophy. Cell Death & Disease, 14(2), 162.
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Publication 2023
Citrate (si)-Synthase Electron Transport Complex III Mitochondria NADH Dehydrogenase Complex 1 Oxidase, Cytochrome-c SDHD protein, human Skeletal Muscles Spectrophotometry Tromethamine
5
Molecular Dynamics Simulations of DPP III Enzyme
All simulations were carried out using the AMBER20 suite of programs [29 (link)].
System minimization was performed in 3 cycles, with 1500, 2500, and 1500 steps for the ligand-free protein structures and for DPP III complexes with Leu-enkephalin and tynorphin, whereas for the complexes with Arg2-2NA and valorphin, for which X-ray structures are not available, an additional minimization cycle (4500 steps) was conducted without any constrains. In the first cycle, water molecules were relaxed while the rest of the system was harmonically restrained with a force constant of 32 kcal mol−1 Å−2. In the second and third cycles, the protein and peptide backbone atoms were restrained with force constants of 12 kcal mol−1 Å−2 and 6 kcal mol−1 Å−2, respectively.
The energy-optimized systems were heated to 300 K (30 ps, NVT ensemble), and the density was equilibrated (970 ps, NpT ensemble). The equilibrated systems were simulated for 1 μs under NpT conditions. During heating and equilibration, the time step was 1 fs, and during the productive MD simulations, it was 2 fs. The SHAKE algorithm was used to constrain covalent bonds with hydrogen atoms. The pressure was maintained at 1 atm using the Berendsen barostat [30 (link)], and the system temperature was kept constant at 300 K using the Langevin thermostat [31 (link)]. Simulations were performed using periodic boundary conditions (PBC) with a cutoff of 11 Å, and the particle mesh Ewald (PME) method was used to calculate long-range electrostatic interactions [32 (link),33 (link)]. Details of the MD simulations can be found in our previous publication [18 (link)]. To allow relaxation of the protein by binding a longer (hepta-peptide) ligand instead of a shorter one (penta-peptide), we restrained valorphin residues at the P2, P1, and P1’ positions and the protein residues E316, Y318, and H568 with the harmonic force constant of 32 kcal mol−1 Å−2 during heating, solvent density equilibration, and during 10 ns of MD simulations at 300 K of wild-type and mutant enzyme complexes’ MD simulations. Then, the systems were gradually relaxed in 4 series of 10 ns MD simulations at 300 K. In the first stage, the side chains of protein residues E316, Y318, and H568 were relaxed; in the second and third stages, the side chains of peptide residues P2, P1, and P1’ were also relaxed; in the fourth stage, only the backbone atoms of peptide residues P2, P1, and P1’ were restrained. These were followed by 1 μs of unconstrained MD simulations.
Tomić A., Karačić Z, & Tomić S. (2023). Influence of Mutations of Conserved Arginines on Neuropeptide Binding in the DPP III Active Site. Molecules, 28(4), 1976.
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Publication 2023
Electron Transport Complex III Electrostatics Enkephalin, Leucine Familial Mediterranean Fever Hydrogen Bonds Ligands Multienzyme Complexes P2 peptide Peptides Pressure Proteins Radiography Solvents Tetranitrate, Pentaerythritol Tremor tynorphin valorphin Vertebral Column

Top products related to «Electron Transport Complex III»

1
Oxygraph 2k by Oroboros
Sourced in Austria
The Oxygraph-2k is a high-performance respirometer designed for precise measurement of oxygen consumption and production in biological samples. It provides real-time monitoring of oxygen levels, making it a valuable tool for researchers in the fields of cell biology, physiology, and bioenergetics.
2
Antimycin a by Merck Group
Sourced in United States, Germany, Italy, United Kingdom, Sao Tome and Principe, China, Japan, Macao, France, Belgium
Antimycin A is a chemical compound that acts as a potent inhibitor of mitochondrial respiration. It functions by blocking the electron transport chain, specifically by interfering with the activity of the cytochrome bc1 complex. This disruption in the respiratory process leads to the inhibition of cellular respiration and energy production within cells.
3
Xf24 extracellular flux analyzer by Agilent Technologies
Sourced in United States, France
The XF24 Extracellular Flux Analyzer is a lab equipment product from Agilent Technologies. It is designed to measure the oxygen consumption rate and extracellular acidification rate of cells in real-time.
4
Oligomycin by Merck Group
Sourced in United States, Germany, United Kingdom, Italy, Sao Tome and Principe, Japan, Macao, France, China, Belgium, Canada, Austria
Oligomycin is a laboratory product manufactured by Merck Group. It functions as an inhibitor of the mitochondrial F1F0-ATP synthase enzyme complex, which is responsible for the synthesis of adenosine triphosphate (ATP) in cells. Oligomycin is commonly used in research applications to study cellular bioenergetics and mitochondrial function.
5
Rotenone by Merck Group
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Rotenone is a naturally occurring insecticide and piscicide derived from the roots of certain tropical plants. It is commonly used as a research tool in laboratory settings to study cellular processes and mitochondrial function. Rotenone acts by inhibiting the electron transport chain in mitochondria, leading to the disruption of cellular respiration and energy production.
6
Seahorse xf24 extracellular flux analyzer by Agilent Technologies
Sourced in United States, China
The Seahorse XF24 Extracellular Flux Analyzer is a lab equipment product designed to measure the metabolic activity of cells. It measures the oxygen consumption rate and extracellular acidification rate of cells in a 24-well microplate format.
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Seahorse xf cell mito stress test kit by Agilent Technologies
Sourced in United States, Germany, Canada
The Seahorse XF Cell Mito Stress Test Kit is a laboratory equipment product designed to measure mitochondrial function in live cells. It provides real-time analysis of key parameters such as oxygen consumption rate and extracellular acidification rate, which are indicators of cellular respiration and metabolic activity.
8
Xf cell mito stress test kit by Agilent Technologies
Sourced in United States, United Kingdom
The XF Cell Mito Stress Test Kit is a laboratory equipment product from Agilent Technologies designed to measure mitochondrial function in live cells. It provides real-time analysis of key parameters related to cellular respiration and energy production.
9
Mitochondrial complex 3 activity assay kit by Abcam
Sourced in United States
The Mitochondrial Complex III Activity Assay Kit is a laboratory tool designed to measure the activity of Complex III, also known as the cytochrome c reductase, within the electron transport chain of mitochondria. This kit provides a quantitative assay to evaluate the enzymatic activity of Complex III in biological samples.
10
Antimycin by Merck Group
Sourced in United States, Germany
Antimycin is a laboratory product manufactured by Merck Group. It is a respiratory inhibitor that functions by interfering with the electron transport chain in mitochondria. The core function of Antimycin is to disrupt cellular respiration.

More about "Electron Transport Complex III"

Electron Transport Complex III, also known as the cytochrome bc1 complex, is a crucial component of the mitochondrial electron transport chain.
This complex, often abbreviated as Complex III or ETC III, plays a central role in cellular respiration by catalyzing the oxidation of ubiquinol and the reduction of cytochrome c, thereby generating a proton gradient that drives ATP synthesis.
Research into the structure, function, and regulation of Electron Transport Complex III has implications for understanding energy metabolism, mitochondrial dysfunction, and various disease states.
The Oxygraph-2k is a powerful tool used to measure oxygen consumption rates, which can provide insights into the activity of Electron Transport Complex III.
Antimycin A, a specific inhibitor of Complex III, is often used in research to study its function and impact on cellular processes.
The XF24 Extracellular Flux Analyzer and the Seahorse XF Cell Mito Stress Test Kit are also valuable instruments that can be used to assess mitochondrial respiration, including the activity of Electron Transport Complex III.
Other key molecules and assays related to Electron Transport Complex III research include Oligomycin, which inhibits ATP synthase, and Rotenone, which inhibits Complex I of the electron transport chain.
The Seahorse XF24 Extracellular Flux Analyzer and the XF Cell Mito Stress Test Kit provide comprehensive tools for evaluating mitochondrial function and the role of Electron Transport Complex III.
Additionally, the Mitochondrial Complex III Activity Assay Kit offers a specific and reliable method for measuring the activity of this crucial complex.
PubCompare.ai's cutting-edge AI-driven protocol optimization can help researchers navigate the vast landscape of literature, pre-prints, and patents to uncover the best protocols and products for their Electron Transport Complex III research needs.
By seamlessly integrating these advanced tools and technologies, researchers can accelerate their discoveries and gain deeper insights into the essential role of Electron Transport Complex III in energy metabolism and mitochondrial function.