An antibiotic substance produced by Streptomyces species. It inhibits mitochondrial respiration and may deplete cellular levels of ATP. Antimycin A1 has been used as a fungicide, insecticide, and miticide. (From Merck Index, 12th ed)
A multisubunit enzyme complex that contains CYTOCHROME B GROUP; CYTOCHROME C1; and iron-sulfur centers. It catalyzes the oxidation of ubiquinol to UBIQUINONE, and transfers the electrons to CYTOCHROME C. In MITOCHONDRIA the redox reaction is coupled to the transport of PROTONS across the inner mitochondrial membrane.
A botanical insecticide that is an inhibitor of mitochondrial electron transport.
The process by which ELECTRONS are transported from a reduced substrate to molecular OXYGEN. (From Bennington, Saunders Dictionary and Encyclopedia of Laboratory Medicine and Technology, 1984, p270)
The 8-hydroxy derivatives inhibit various enzymes and their halogenated derivatives, though neurotoxic, are used as topical anti-infective agents, among other uses.
Inorganic salts of HYDROGEN CYANIDE containing the -CN radical. The concept also includes isocyanides. It is distinguished from NITRILES, which denotes organic compounds containing the -CN radical.
A lipid-soluble benzoquinone which is involved in ELECTRON TRANSPORT in mitochondrial preparations. The compound occurs in the majority of aerobic organisms, from bacteria to higher plants and animals.
Acrylic acids or acrylates which are substituted in the C-2 position with a methyl group.
Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)
A closely related group of toxic substances elaborated by various strains of Streptomyces. They are 26-membered macrolides with lactone moieties and double bonds and inhibit various ATPases, causing uncoupling of phosphorylation from mitochondrial respiration. Used as tools in cytochemistry. Some specific oligomycins are RUTAMYCIN, peliomycin, and botrycidin (formerly venturicidin X).
Derivatives of SUCCINIC ACID. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain a 1,4-carboxy terminated aliphatic structure.
Hemeproteins whose characteristic mode of action involves transfer of reducing equivalents which are associated with a reversible change in oxidation state of the prosthetic group. Formally, this redox change involves a single-electron, reversible equilibrium between the Fe(II) and Fe(III) states of the central iron atom (From Enzyme Nomenclature, 1992, p539). The various cytochrome subclasses are organized by the type of HEME and by the wavelength range of their reduced alpha-absorption bands.
Chemical agents that uncouple oxidation from phosphorylation in the metabolic cycle so that ATP synthesis does not occur. Included here are those IONOPHORES that disrupt electron transfer by short-circuiting the proton gradient across mitochondrial membranes.
NAD(P)H:(quinone acceptor) oxidoreductases. A family that includes three enzymes which are distinguished by their sensitivity to various inhibitors. EC 1.6.99.2 (NAD(P)H DEHYDROGENASE (QUINONE);) is a flavoprotein which reduces various quinones in the presence of NADH or NADPH and is inhibited by dicoumarol. EC 1.6.99.5 (NADH dehydrogenase (quinone)) requires NADH, is inhibited by AMP and 2,4-dinitrophenol but not by dicoumarol or folic acid derivatives. EC 1.6.99.6 (NADPH dehydrogenase (quinone)) requires NADPH and is inhibited by dicoumarol and folic acid derivatives but not by 2,4-dinitrophenol.
Cytochromes (electron-transporting proteins) with protoheme (HEME B) as the prosthetic group.
A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471).
A barbiturate with hypnotic and sedative properties (but not antianxiety). Adverse effects are mainly a consequence of dose-related CNS depression and the risk of dependence with continued use is high. (From Martindale, The Extra Pharmacopoeia, 30th ed, p565)
The rate at which oxygen is used by a tissue; microliters of oxygen STPD used per milligram of tissue per hour; the rate at which oxygen enters the blood from alveolar gas, equal in the steady state to the consumption of oxygen by tissue metabolism throughout the body. (Stedman, 25th ed, p346)
A water-soluble, colorless crystal with an acid taste that is used as a chemical intermediate, in medicine, the manufacture of lacquers, and to make perfume esters. It is also used in foods as a sequestrant, buffer, and a neutralizing agent. (Hawley's Condensed Chemical Dictionary, 12th ed, p1099; McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed, p1851)
A highly poisonous compound that is an inhibitor of many metabolic processes, but has been shown to be an especially potent inhibitor of heme enzymes and hemeproteins. It is used in many industrial processes.
Mitochondria in hepatocytes. As in all mitochondria, there are an outer membrane and an inner membrane, together creating two separate mitochondrial compartments: the internal matrix space and a much narrower intermembrane space. In the liver mitochondrion, an estimated 67% of the total mitochondrial proteins is located in the matrix. (From Alberts et al., Molecular Biology of the Cell, 2d ed, p343-4)
A genus of gram-negative bacteria widely distributed in fresh water as well as marine and hypersaline habitats.
A proton ionophore that is commonly used as an uncoupling agent in biochemical studies.
Chelating agent and inhibitor of cellular respiration.
The 30-kDa membrane-bound c-type cytochrome protein of mitochondria that functions as an electron donor to CYTOCHROME C GROUP in the mitochondrial and bacterial RESPIRATORY CHAIN. (From Enzyme Nomenclature, 1992, p545)
A proton ionophore. It is commonly used as an uncoupling agent and inhibitor of photosynthesis because of its effects on mitochondrial and chloroplast membranes.
The class of all enzymes catalyzing oxidoreduction reactions. The substrate that is oxidized is regarded as a hydrogen donor. The systematic name is based on donor:acceptor oxidoreductase. The recommended name will be dehydrogenase, wherever this is possible; as an alternative, reductase can be used. Oxidase is only used in cases where O2 is the acceptor. (Enzyme Nomenclature, 1992, p9)
Inorganic salts of the hypothetical acid, H3Fe(CN)6.
Organic compounds that contain two nitro groups attached to a phenol.
An anti-gas warfare agent that is effective against Lewisite (dichloro(2-chlorovinyl)arsine) and formerly known as British Anti-Lewisite or BAL. It acts as a chelating agent and is used in the treatment of arsenic, gold, and other heavy metal poisoning.
The various filaments, granules, tubules or other inclusions within mitochondria.
A flavoprotein and iron sulfur-containing oxidoreductase that catalyzes the oxidation of NADH to NAD. In eukaryotes the enzyme can be found as a component of mitochondrial electron transport complex I. Under experimental conditions the enzyme can use CYTOCHROME C GROUP as the reducing cofactor. The enzyme was formerly listed as EC 1.6.2.1.
Molecules or ions formed by the incomplete one-electron reduction of oxygen. These reactive oxygen intermediates include SINGLET OXYGEN; SUPEROXIDES; PEROXIDES; HYDROXYL RADICAL; and HYPOCHLOROUS ACID. They contribute to the microbicidal activity of PHAGOCYTES, regulation of signal transduction and gene expression, and the oxidative damage to NUCLEIC ACIDS; PROTEINS; and LIPIDS.
The mitochondria of the myocardium.
The metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell.
Electron transfer through the cytochrome system liberating free energy which is transformed into high-energy phosphate bonds.
An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.
A pre-emergent herbicide.
The art or process of comparing photometrically the relative intensities of the light in different parts of the spectrum.
A coenzyme composed of ribosylnicotinamide 5'-diphosphate coupled to adenosine 5'-phosphate by pyrophosphate linkage. It is found widely in nature and is involved in numerous enzymatic reactions in which it serves as an electron carrier by being alternately oxidized (NAD+) and reduced (NADH). (Dorland, 27th ed)
Drugs that are chemically similar to naturally occurring metabolites, but differ enough to interfere with normal metabolic pathways. (From AMA Drug Evaluations Annual, 1994, p2033)
A group of cytochromes with covalent thioether linkages between either or both of the vinyl side chains of protoheme and the protein. (Enzyme Nomenclature, 1992, p539)
A group of oxidoreductases that act on NADH or NADPH. In general, enzymes using NADH or NADPH to reduce a substrate are classified according to the reverse reaction, in which NAD+ or NADP+ is formally regarded as an acceptor. This subclass includes only those enzymes in which some other redox carrier is the acceptor. (Enzyme Nomenclature, 1992, p100) EC 1.6.
Amides of salicylic acid.
The rate dynamics in chemical or physical systems.
A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials.
Inorganic salts of the hypothetical acid ferrocyanic acid (H4Fe(CN)6).
Cytochromes of the b group that have alpha-band absorption of 563-564 nm. They occur as subunits in MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX III.
The terms, expressions, designations, or symbols used in a particular science, discipline, or specialized subject area.
Freedom from exposure to danger and protection from the occurrence or risk of injury or loss. It suggests optimal precautions in the workplace, on the street, in the home, etc., and includes personal safety as well as the safety of property.
Unforeseen occurrences, especially injuries in the course of work-related activities.
Databases devoted to knowledge about specific chemicals.
Exclusive legal rights or privileges applied to inventions, plants, etc.

Characterization of a leukotriene C4 export mechanism in human platelets: possible involvement of multidrug resistance-associated protein 1. (1/715)

Platelets express leukotriene (LT) C4 synthase and can thus participate in the formation of bioactive LTC4. To further elucidate the relevance of this capability, we have now determined the capacity of human platelets to export LTC4. Endogenously formed LTC4 was efficiently released from human platelets after incubation with LTA4 at 37 degrees C, whereas only 15% of produced LTC4 was exported when the cells were incubated at 0 degrees C. The activation energy of the process was calculated to 49.9 +/- 7.7 kJ/mol, indicating carrier-mediated LTC4 export. This was also supported by the finding that the transport was saturable, reaching a maximal export rate of 470 +/- 147 pmol LTC4/min x 10(9) platelets. Furthermore, markedly suppressed LTC4 transport was induced by a combination of the metabolic inhibitors antimycin A and 2-deoxyglucose, suggesting energy-dependent export. The presence in platelets of multidrug resistance-associated protein 1 (MRP1), a protein described to be an energy-dependent LTC4 transporter in various cell types, was demonstrated at the mRNA and protein level. Additional support for a role of MRP1 in platelet LTC4 export was obtained by the findings that the process was inhibited by probenecid and the 5-lipoxygenase-activating protein (FLAP) inhibitor, MK-886. The present findings further support the physiological relevance of platelet LTC4 production.  (+info)

Ubiquinol:cytochrome c oxidoreductase. Effects of inhibitors on reverse electron transfer from the iron-sulfur protein to cytochrome b. (2/715)

The effects of inhibitors on the reduction of the bis-heme cytochrome b of ubiquinol: cytochrome c oxidoreductase (complex III, bc1 complex) has been studied in bovine heart submitochondrial particles (SMP) when cytochrome b was reduced by NADH and succinate via the ubiquinone (Q) pool or by ascorbate plus N,N,N', N'-tetramethyl-p-phenylenediamine via cytochrome c1 and the iron-sulfur protein of complex III (ISP). The inhibitors used were antimycin (an N-side inhibitor), beta-methoxyacrylate derivatives, stigmatellin (P-side inhibitors), and ethoxyformic anhydride, which modifies essential histidyl residues in ISP. In agreement with our previous findings, the following results were obtained: (i) When ISP/cytochrome c1 were prereduced or SMP were treated with a P-side inhibitor, the high potential heme bH was fully and rapidly reduced by NADH or succinate, whereas the low potential heme bL was only partially reduced. (ii) Reverse electron transfer from ISP/c1 to cytochrome b was inhibited more by antimycin than by the P-side inhibitors. This reverse electron transfer was unaffected when, instead of normal SMP, Q-extracted SMP containing 200-fold less Q (0. 06 mol Q/mol cytochrome b or c1) were used. (iii) The cytochrome b reduced by reverse electron transfer through the leak of a P-side inhibitor was rapidly oxidized upon subsequent addition of antimycin. This antimycin-induced reoxidation did not happen when Q-extracted SMP were used. The implications of these results on the path of electrons in complex III, on oxidant-induced extra cytochrome b reduction, and on the inhibition of forward electron transfer to cytochrome b by a P-side plus an N-side inhibitor have been discussed.  (+info)

Light-induced oxidation-reduction reactions of cytochromes in the green sulfur photosynthetic bacterium Prosthecochloris aesturarii. (3/715)

The light-induced oxidation-reduction reactions of cytochromes in intact cells, starved cells, and chlorobium vesicle fractions of the green sulfur photosynthetic bacterium Prosthecochloris aesturarii were studied under anaerobic conditions. On the basis of both kinetic and spectral properties, at least three cytochrome species were found to be involved in the light-induced oxidation-reduction reactions of intact cells. These cytochromes were designated according to the positions of alpha-band maxima as C555 (rapid and slow components) and C552 (intermediate). By comparing the light-minus-dark difference spectra with the reduced-minus-oxidized difference spectra of purified cytochromes of this organism, rapid component C555 and intermediate component C552 are suggested to correspond to the purified cytochromes c-555(550) and c-551.5, respectively. Although the identity of the slow-phase component is uncertain, one possibility is that the slow phase is due to the bound form of c-555(550). In substrate-depleted (starved) cells, only one cytochrome species, C555 remained in the reduced state in the dark and oxidized upon actinic illumination. This corresponds to the rapid C555 component in intact cells. In the case of chlorobium vesicle fractions, one cytochrome species having an alpha-band maximum at 554 nm was oxidized by actinic light. The effects of several inhibitors on the absorbance changes of intact cells were studied. Antimycin A decreased the rate of the dark reduction of rapid C555 component. The complex effects of CCCP (carbonyl cyanide m-chlorophenylhydrazone) on the oxidation-reduction reactions of cytochromes were interpreted as the results of inhibition of the electron donation to oxidized C552 and C555 (slow), and a shift of the dark steady-state redox levels of cytochromes. Based on these findings, it is suggested that the rapid C555 component is located in a cyclic electron transfer pathway. The other two cytochromes, C552 and C555 (slow), may be located in non-cyclic electron transfer pathways and receive electrons from exogenous substrates such as sodium sulfide. A tentative scheme for the electron transfer system in Prosthecochloris aestuarii is presented and its nature is discussed.  (+info)

Roles of Na(+)-Ca2+ exchange and of mitochondria in the regulation of presynaptic Ca2+ and spontaneous glutamate release. (4/715)

The release of neurotransmitter from presynaptic terminals depends on an increase in the intracellular Ca2+ concentration ([Ca2+]i). In addition to the opening of presynaptic Ca2+ channels during excitation, other Ca2+ transport systems may be involved in changes in [Ca2+]i. We have studied the regulation of [Ca2+]i in nerve terminals of hippocampal cells in culture by the Na(+)-Ca2+ exchanger and by mitochondria. In addition, we have measured changes in the frequency of spontaneous excitatory postsynaptic currents (sEPSC) before and after the inhibition of the exchanger and of mitochondrial metabolism. We found rather heterogeneous [Ca2+]i responses of individual presynaptic terminals after inhibition of Na(+)-Ca2+ exchange. The increase in [Ca2+]i became more uniform and much larger after additional treatment of the cells with mitochondrial inhibitors. Correspondingly, sEPSC frequencies changed very little when only Na(+)-Ca2+ exchange was inhibited, but increased dramatically after additional inhibition of mitochondria. Our results provide evidence for prominent roles of Na(+)-Ca2+ exchange and mitochondria in presynaptic Ca2+ regulation and spontaneous glutamate release.  (+info)

Interorganelle signaling is a determinant of longevity in Saccharomyces cerevisiae. (5/715)

Replicative capacity, which is the number of times an individual cell divides, is the measure of longevity in the yeast Saccharomyces cerevisiae. In this study, a process that involves signaling from the mitochondrion to the nucleus, called retrograde regulation, is shown to determine yeast longevity, and its induction resulted in postponed senescence. Activation of retrograde regulation, by genetic and environmental means, correlated with increased replicative capacity in four different S. cerevisiae strains. Deletion of a gene required for the retrograde response, RTG2, eliminated the increased replicative capacity. RAS2, a gene previously shown to influence longevity in yeast, interacts with retrograde regulation in setting yeast longevity. The molecular mechanism of aging elucidated here parallels the results of genetic studies of aging in nematodes and fruit flies, as well as the caloric restriction paradigm in mammals, and it underscores the importance of metabolic regulation in aging, suggesting a general applicability.  (+info)

Oxygen sensing in yeast: evidence for the involvement of the respiratory chain in regulating the transcription of a subset of hypoxic genes. (6/715)

Oxygen availability affects the transcription of a number of genes in nearly all organisms. Although the molecular mechanisms for sensing oxygen are not precisely known, heme is thought to play a pivotal role. Here, we address the possibility that oxygen sensing in yeast, as in mammals, involves a redox-sensitive hemoprotein. We have found that carbon monoxide (CO) completely blocks the anoxia-induced expression of two hypoxic genes, OLE1 and CYC7, partially blocks the induction of a third gene, COX5b, and has no effect on the expression of other hypoxic or aerobic genes. In addition, transition metals (Co and Ni) induce the expression of OLE1 and CYC7 in a concentration-dependent manner under aerobic conditions. These findings suggest that the redox state of an oxygen-binding hemoprotein is involved in controlling the expression of at least two hypoxic yeast genes. By using mutants deficient in each of the two major yeast CO-binding hemoproteins (cytochrome c oxidase and flavohemoglobin), respiratory inhibitors, and cob1 and rho0 mutants, we have found that the respiratory chain is involved in the anoxic induction of these two genes and that cytochrome c oxidase is likely the hemoprotein "sensor." Our findings also indicate that there are at least two classes of hypoxic genes in yeast (CO sensitive and CO insensitive) and imply that multiple pathways/mechanisms are involved in modulating the expression of hypoxic yeast genes.  (+info)

Role of tyrosine phosphorylation in the reassembly of occludin and other tight junction proteins. (7/715)

After the simulation of anoxia by ATP depletion of MDCK cell monolayers with metabolic inhibitors, the tight junction (TJ) is known to become structurally perturbed, leading to loss of the permeability barrier. Peripheral TJ proteins such as zonula occludens 1 (ZO-1), ZO-2, and cingulin become extremely insoluble and associate into large macromolecular complexes (T. Tsukamoto and S. K. Nigam. J. Biol. Chem. 272: 16133-16139, 1997). For up to 3 h, this process is reversible by ATP repletion. We now show that the reassembly process depends on tyrosine phosphorylation. Recovery of transepithelial electrical resistance in ATP-replete monolayers was markedly inhibited by the tyrosine kinase inhibitor, genistein. Indirect immunofluorescence revealed a decrease in staining of occludin, a membrane component of the TJ, in the region of the TJ after ATP depletion, which reversed after ATP repletion; this reversal process was inhibited by genistein. Examination of the Triton X-100 solubilities of occludin and several nonmembrane TJ proteins revealed a shift of occludin and nonmembrane TJ proteins into an insoluble pool following ATP depletion. These changes reversed after ATP repletion, and the movement of insoluble occludin, ZO-1, and ZO-2 back into the soluble pool was again via a genistein-sensitive mechanism. Rate-zonal centrifugation analyses of detergent-soluble TJ proteins showed a reversible increase in higher density fractions following ATP depletion-repletion, although this change was not affected by genistein. In 32P-labeled cells, dephosphorylation of all studied TJ proteins was observed during ATP depletion, followed by rephosphorylation during ATP repletion; rephosphorylation of occludin was inhibited by genistein. Furthermore, during the ATP repletion phase, tyrosine phosphorylation of Triton X-100-insoluble occludin, which is localized at the junction, as well as ZO-2, p130/ZO-3 (though not ZO-1), and other proteins was evident; this tyrosine phosphorylation was completely inhibited by genistein. This indicates that tyrosine kinase activity is necessary for TJ reassembly during ATP repletion and suggests an important role for the tyrosine phosphorylation of occludin, ZO-2, p130/ZO-3, and possibly other proteins in the processes involved in TJ (re)formation.  (+info)

A mechanism for the synergistic antimalarial action of atovaquone and proguanil. (8/715)

A combination of atovaquone and proguanil has been found to be quite effective in treating malaria, with little evidence of the emergence of resistance when atovaquone was used as a single agent. We have examined possible mechanisms for the synergy between these two drugs. While proguanil by itself had no effect on electron transport or mitochondrial membrane potential (DeltaPsim), it significantly enhanced the ability of atovaquone to collapse DeltaPsim when used in combination. This enhancement was observed at pharmacologically achievable doses. Proguanil acted as a biguanide rather than as its metabolite cycloguanil (a parasite dihydrofolate reductase [DHFR] inhibitor) to enhance the atovaquone effect; another DHFR inhibitor, pyrimethamine, also had no enhancing effect. Proguanil-mediated enhancement was specific for atovaquone, since the effects of other mitochondrial electron transport inhibitors, such as myxothiazole and antimycin, were not altered by inclusion of proguanil. Surprisingly, proguanil did not enhance the ability of atovaquone to inhibit mitochondrial electron transport in malaria parasites. These results suggest that proguanil in its prodrug form acts in synergy with atovaquone by lowering the effective concentration at which atovaquone collapses DeltaPsim in malaria parasites. This could explain the paradoxical success of the atovaquone-proguanil combination even in regions where proguanil alone is ineffective due to resistance. The results also suggest that the atovaquone-proguanil combination may act as a site-specific uncoupler of parasite mitochondria in a selective manner.  (+info)

Objective: Mitochondrial dysfunction is often associated with various disorders such as diabetes, Alzheimers etc. Reactive oxygen species (ROS), aging, and reducti..
In Candida albicans, cyanide and antimycin A inhibited K(+) transport, not only with ethanol-O2 as the substrate, but also with glucose. The reason for this was that they inhibited not only respiration, but also fermentation, decreasing ATP production. Measurements of oxygen levels in cell suspensions allowed identification of the electron pathways involved. NADH fluorescence levels increased in the presence of the inhibitors, indirectly indicating lower levels of NAD(+) and so pointing to glyceraldehyde-3-phosphate dehydrogenase as the limiting step responsible for the inhibition of glycolysis, which was confirmed by the levels of glycolytic intermediaries. The cyanide effect could be reversed by hydrogen peroxide, mainly due to an activity by which H2O2 can be reduced by electrons flowing from NADH through a pathway that can be inhibited by antimycin A, and appears to be a cytochrome c peroxidase. Therefore, the inhibition of glycolysis by the respiratory inhibitors seems to be due to the ...
Antimycin A1 is the most hydrophobic of the four analogues of the antimycin A complex. Although broadly active as respiration inhibitors, more recent investigation has highlighted the importance of individual members of the complex as bioprobes ...
Antimycin A | C28H40N2O9 | CID 14957 - structure, chemical names, physical and chemical properties, classification, patents, literature, biological activities, safety/hazards/toxicity information, supplier lists, and more.
This is concordant with the actuality that Isa1p has not been described as collaborating in the assembly of 2Fe?S facilities, which is the type of ISC existing
The transition of the bacterial culture into the stationary growth phase is accompanied by an appearance of cyanide-resistant respiration. Chloramphenicol inhibits the development of cyanide-resistant respiration. The cyanide-resistant oxidase is localized in the bacterial membrane. Its appearance is not due to the quantitative and qualitative changes of flavins, non-heme iron, ubiquinone and cytochromes of the b and c types, but is accompanied by an increase in the copper content of the membrane preparations. Neither cyanide-sensitive, nor cyanide-resistant chains of the bacterial electron transfer contain cytochromes of the a type. The cyanide-resistant oxidase accepts electrons at the ubiquinone--cytochrome b level of the main respiratory chain. The cyanide-resistant respiration is not accompanied by a formation of hydrogen peroxide. Cytochrome o performs the function of cyanide-sensitive oxidase. The nature of cyanide-resistant oxidase still remains obscure. ...
1PP9: Binding of the Respiratory Chain Inhibitor Antimycin to the Mitochondrial bc(1) Complex: A New Crystal Structure Reveals an Altered Intramolecular Hydrogen-bonding Pattern.
Hes a famous doctor and Instagram celeb, and when faced with an in-flight emergency, Dr. Mike was forced to spring into action.
Toxoplasma gondii is an apicomplexan parasite that causes fatal and debilitating brain and eye disease. Endochin-like-quinolones (ELQs) are preclinical compounds that are efficacious against apicomplexan-caused diseases including toxoplasmosis, malaria and babesiosis. Of the ELQs, ELQ-316 has demonstrated the greatest efficacy against acute and chronic experimental toxoplasmosis. Although genetic analyses in other organisms have highlighted the importance of the cytochrome bc1 complex Qi site for ELQ sensitivity, the mechanism of action of ELQs against T. gondii and the mechanism of ELQ-316 remains unknown. Here we describe the selection and genetic characterization of T. gondii clones resistant to ELQ-316. A T. gondii strain selected under ELQ-316 drug pressure was found to possess a Thr222-Pro amino acid substitution that confers 49-fold resistance to ELQ-316 and 19-fold resistance to antimycin, a well-characterized Qi site inhibitor. These findings provide further evidence for ELQ Qi site ...
Myxothiazol, an antifungal antibiotic, is a mitochondrial electron transport chain complex III (bc1 complex) inhibitor. Myxothiazol inhibits the growth of many yeasts and fungi at concentrations between 0.01 and 3 μg/ml. - Mechanism of Action & Protocol.
Mitochondria in oligodendrocyte progenitor cells (OPs) Dtake up and release cytosolic Ca2+ during agonist-evoked Ca2+ waves, but it is not clear whether or how they regulate Ca2+ signaling in OPs. We asked whether mitochondria. play an active role during agonist-evoked Ca2+ release from intracellular stores. Ca2+ puffs, wave initiation, and wave propagation were measured in fluo-4 loaded OP processes using linescan confocal microscopy. Mitochondrial depolarization, measured by tetramethyl rhodamine ethyl ester (TMRE) fluorescence, accompanied Ca2+ puffs and waves. in addition, waves initiated only where mitochondria were localized. To determine whether energized mitochondria were necessary for wave generation, we blocked mitochondrial function with the electron transport chain inhibitor antimycin A (AA) in combination with oligomycin. AA decreased wave speed and puff probability. These effects were not due to global changes in ATP. We found that AA increased cytosolic Ca2+ markedly reduced ...
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Fingerprint Dive into the research topics of High endoplasmic reticulum activity renders Multiple myeloma cells hypersensitive to mitochondrial inhibitors. Together they form a unique fingerprint. ...
Now, theyve shown that the same holds true in a living animal. Importantly, ubiquitous Ciona AOX activity had no apparent ill effects for the flies. Quite the contrary, mitochondria taken from AOX-expressing flies showed significant resistance to cyanide, and the flies partially resisted both cyanide and antimycin. AOX also rescued the movement defect and excess production of reactive oxygen species by mitochondria in flies with a mutant version of a gene known as dj-1b, which is the fly equivalent to the human Parkinsons disease gene DJ1 ...
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Mutations in the assembly chaperone BCS1L constitute a major cause of mitochondrial complex III deficiency. We studied the presence of BCS1L mutations in a complex III-deficient patient with metabolic acidosis, liver failure, and tubulopathy. A previously reported mutation, p.R56X, was identified in one BCS1L allele, and two novel heterozygous mutations, g.1181A|G and g.1164C|G, were detected in the second allele. The g.1181A|G mutation generated an alternative splicing site in the BCS1L transcript, causing a 19-nucleotides deletion in its 5UTR region. Decreased BCS1L mRNA and protein levels, and a respiratory chain complex III assembly impairment, determine a pathogenic role for the novel BCS1L mutations.
Supplementary MaterialsS1 Raw images: (PDF) pone. but not male MLEC. In contrast, treatment with mitochondrial respiratory Complex III inhibitor Antimycin A (AA, 50M) mediated severe necrosis specifically in male MLEC, while female cells again responded primarily by apoptosis. The same effect with female cells responding to the stress by apoptosis and male cells responding by necrosis was confirmed in starved pulmonary endothelial cells isolated from human donors. Elevated necrosis seen in male cells was associated with a significant release of damage-associated alarmin, HMGB1. No stimuli induced a significant elevation of HMGB1 secretion in females. We conclude that male cells appear to be protected against mild stress conditions, such as hypoxia, possibly due to increased mitochondrial respiration. In contrast, they are more sensitive to impaired mitochondrial function, to which they respond by necrotic death. Necrosis in male vascular cells releases a significant amount of HMGB1 that could ...
1. Pigeon heart mitochondria produce H2O2 at a maximal rate of about 20nmol/min per mg of protein. 2. Succinate-glutamate and malate-glutamate are substrates which are able to support maximal H2O2 production rates. With malate-glutamate, H2O2 formation is sensitive to rotenone. Endogenous substrate, octanoate, stearoyl-CoA and palmitoyl-carnitine are by far less efficient substrates. 3. Antimycin A exerts a very pronounced effect in enhancing H2O2 production in pigeon heart mitochondria; 0.26nmol of antimycin A/mg of protein and the addition of an uncoupler are required for maximal H2O2 formation. 4. In the presence of endogenous substrate and of antimycin A, ATP decreases and uncoupler restores the rates of H2O2 formation. 5. Reincorporation of ubiquinone-10 and ubiquinone-3 to ubiquinone-depleted pigeon heart mitochondria gives a system in which H2O2 production is linearly related to the incorporated ubiquinone. 6. The generation of H2O2 by pigeon heart mitochondria in the presence of ...
SUIT-009 is a short protocol for simultaneous determination of O2 flux and the rate of H2O2 production (H2O2 flux) on isolated mitochondria, tissue homogenate (except of liver) and permeabilized cells. Succinate (S) supports the reverse electron transfer (RET)-related H2O2 production in the LEAK state. Pyruvate (P) promotesNADH-pathway (N), and usually in the presence of ADP, H2O2 flux is not increased further. Antimycin A (Ama) inhibits Complex III (CIII) and could increase the H2O2 flux. The sensitivity of the Amplex UltraRed® assay (for determining H2O2 production) changes over the experimental time and upon addition of chemicals. To correct H2O2 flux for the sensitivity changes several H2O2 calibration steps are done during the experiment. The measurement is carried out in MiR05-Kit at 37 °C. For O2-Application, apply SUIT-009 O2 mt D015 or SUIT-009 O2 ce-pce D016; for O2 and H2O2 measurements (AmR), apply SUIT-009 AmR mt D021 or SUIT-009 AmR ce-pce D019. ...
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What is the difference between Ubiquinol and regular CoQ10? Ubiquinol is the most readily absorbed form of CoQ10 and is one of the most powerful fat-soluble antioxidants in the body. Ubiquinol is also the major form of CoQ10 in the body (over 95 ...
What is the difference between Ubiquinol and regular CoQ10? Ubiquinol is the most readily absorbed form of CoQ10 and is one of the most powerful fat-soluble antioxidants in the body. Ubiquinol is also the major form of CoQ10 in the body (over 95 ...
The mitochondrion is emerging as a key organelle in stem cell biology, acting as a regulator of stem cell pluripotency and differentiation. In this study we sought to understand the effect of mitochondrial complex III inhibition during neuronal differentiation of mouse embryonic stem cells. When exposed to antimycin A, a specific complex III inhibitor, embryonic stem cells failed to differentiate into dopaminergic neurons, maintaining high Oct4 levels even when subjected to a specific differentiation protocol. Mitochondrial inhibition affected distinct populations of cells present in culture, inducing cell loss in differentiated cells, but not inducing apoptosis in mouse embryonic stem cells. A reduction in overall proliferation rate was observed, corresponding to a slight arrest in S phase. Moreover, antimycin A treatment induced a consistent increase in HIF-1α protein levels. The present work demonstrates that mitochondrial metabolism is critical for neuronal differentiation and emphasizes that
Component of the ubiquinol-cytochrome c oxidoreductase, a multisubunit transmembrane complex that is part of the mitochondrial electron transport chain which drives oxidative phosphorylation. The respiratory chain contains 3 multisubunit complexes succinate dehydrogenase (complex II, CII), ubiquinol-cytochrome c oxidoreductase (cytochrome b-c1 complex, complex III, CIII) and cytochrome c oxidase (complex IV, CIV), that cooperate to transfer electrons derived from NADH and succinate to molecular oxygen, creating an electrochemical gradient over the inner membrane that drives transmembrane transport and the ATP synthase. The cytochrome b-c1 complex catalyzes electron transfer from ubiquinol to cytochrome c, linking this redox reaction to translocation of protons across the mitochondrial inner membrane, with protons being carried across the membrane as hydrogens on the quinol. In the process called Q cycle, 2 protons are consumed from the matrix, 4 protons are released into the intermembrane space and 2
MITOCHONDRIAL COMPLEX III DEFICIENCY, NUCLEAR TYPE 4; MC3DN4 description, symptoms and related genes. Get the complete information in our medical sear
The SCOP classification for the Non-heme 11 kDa protein of cytochrome bc1 complex (Ubiquinol-cytochrome c reductase) superfamily including the families contained in it. Additional information provided includes InterPro annotation (if available), Functional annotation, and SUPERFAMILY links to genome assignments, alignments, domain combinations, taxonomic visualisation and hidden Markov model information.
This gene encodes the smallest known component of the ubiquinol-cytochrome c reductase complex, which forms part of the mitochondrial respiratory chain. The encoded protein may function as a binding factor for the iron-sulfur protein in this complex. [provided by RefSeq, Oct 2009 ...
In addition, at Neurovive we have recently experienced another issue that could affect the use of these prodrugs in a rotenone-induced lactate assay and we suggest to formulate the limitation for Snv this way: Snv is a prodrug of succinate for in vitro use with the main application to deliver succinate to living cells in respiratory (oxygen consumption) protocols. Upon intracellular prodrug hydrolysis, formaldehyde is released which, at high concentration, has an inhibitory effect on glycolysis (Tiffert et al 1984). For in vitro experiments dependent of glycolysis and lacatate production as an output measure Snv should be carefully titrated to improve mitochondrial respiration without inhibiting glycolysis, which could be evidenced by restored lactate production following downstream (of CII) inhibition of the electron transfer system (using antimycin A ...
Ubiquinol Acetate Ubiquinol acetate : Reduced form of Co-Q 10 Absorption : Superior Absorption Stability: Very stable form and does not require special storage condition. Bioavailability: More bioavailable than normal ubiquinone. Facility: FSSAI, GMP and FSSC 22000 certified company Ubiquinol Acetate delivers antioxida
Buy UBIQUINOL 100mg NOW - 60 softgels Online.UBIQUINOL by Now Foods is the reduced form of CoQ-10 (coenzyme Q10). Scientific studies have shown it to be the most bioavailable form of CoQ-10 currently on the market.
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QCR6_YEAST] Component of the ubiquinol-cytochrome c reductase complex (complex III or cytochrome b-c1 complex), which is part of the mitochondrial respiratory chain that generates an electrochemical potential coupled to ATP synthesis. The complex couples electron transfer from ubiquinol to cytochrome c. QCR6 may mediate formation of the complex between cytochromes c and c1. [CYB_YEAST] Component of the ubiquinol-cytochrome c reductase complex (complex III or cytochrome b-c1 complex), which is part of the mitochondrial respiratory chain that generates an electrochemical potential coupled to ATP synthesis. The complex couples electron transfer from ubiquinol to cytochrome c. [QCR7_YEAST] Component of the ubiquinol-cytochrome c reductase complex (complex III or cytochrome b-c1 complex), which is part of the mitochondrial respiratory chain that generates an electrochemical potential coupled to ATP synthesis. The complex couples electron transfer from ubiquinol to cytochrome c. QCR7 is involved in ...
2-Heptyl-4-hydroxyquinoline N-oxide (HQNO), a major secondary metabolite and virulence factor produced by the opportunistic pathogen Pseudomonas...
Renal proximal tubules are the major target of toxicant and ischemic injury in the kidney. Because mitochondria play a crucial role in ATP generation and survival of RPTCs, mitochondrial dysfunction caused by toxicant exposure or ischemia leads to RPTC injury and death and plays a major role in the development of acute kidney injury (Abid et al., 2005; Cachofeiro et al., 2008; Koyner et al., 2008). Oxidative stress is believed to be an important mechanism of toxicant- and ischemia-induced injury to RPTCs (Abid et al., 2005; Cachofeiro et al., 2008; Koyner et al., 2008). Therefore, we hypothesized that GT3, a potent antioxidant, may limit or prevent mitochondrial dysfunction, energy deficits, and cell death caused by oxidant exposure. Our data demonstrate that GT3 is taken up by RPTCs by a process that is saturated within 24 h, which suggests that GT3 is not taken up by simple diffusion. The saturation of GT3 uptake is not caused by depletion of GT3 from the cell culture media. At this point of ...
However, we found no difference in the AО 42 protein level between the Vps18 Ohw and Ctrl mice (data not shown). HeВ did not give a specific timeframe for a launch в saying only that the tech is working todayв. If you are currently using a Dedicated server and thinking switching to a VPS we recommend to think twice. You will also have to modify the etcopenvpn file later to point to the correctcrt andkey files. Over 90 of the OMIMs operating expenses go to salary support for MD and PhD science writers and biocurators. As a control, how to build a secure linux server expressing GFPвUVRAG dblA at a similar level to WT Free sms server gateway failed to produce any reactivity with the phosphoвspecific antibodies under any condition. How to configure vpn access on server 2008 can get in touch with our fully qualified technical support via Live Chat, Phone, or Hkw around the clock 24x7x365. ProSpecs products are furnished for LABORATORY RESEARCH USE Bild. If not for antimycin A, the yeast might ...
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Description The essential nutrient Coenzyme Q10 is a necessary component of cellular energy production and respiration. It is a component of the mitochondrial electron transport system, which supplies the energy required for a variety of physiological functions. CoQ10 provides support to all cells of the body, and is e
Ubiquinone and ubiquinol are the oxidized and reduced variants of the nutrient Coenzyme Q10, reports Meghan Lyons MS. Ubiquinol is produced by the addition of an electron to ubiquinone and vice...
CoQ10 exists in two forms, as ubiquinone (the oxidised CoQ10, spent form) and ubiquinol (the reduced and activated, antioxidant form). In order for CoQ10 to play a role in energy production and exhibit an antioxidant effect, the body must metabolise it to its antioxidant form ubiquinol, a process inhibited with increasing age, nutrient deficiency and some health conditions. Taking CoQ10 as ubiquinone is therefore not as effective as taking CoQ10 as ubiquinol (Kaneka QH™) the body-ready form which has only been available for use in supplements since 2006. Ubiquinol has numerous advantages over ubiquinone and comparing the two forms in therapeutic outcomes far surpasses its oxidised precursor.. Bioavailability When addressing the issue of therapeutics, at first glance the dose of ubiquinol may seem particularly relevant; however, it is the blood plasma level achieved by supplementation that is the significant factor in determining the effectiveness of a treatment. [4] As a lipid-soluble ...
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Various organic hydroperoxides are reduced when added to rat liver mitochondrial suspensions. Succinate increases the rate and duration of the reductions except for linoleic acid hydroperoxide which appears to inhibit its own reduction. 3-Hydroxybutyrate replaces succinate but other reductants used are less effective. The rate of reduction of tert-butyl hydroperoxide by succinate is not inhibited by cyanide but is partly inhibited if antimycin or rotenone are also added; ATP reverses the antimycin inhibition. Other inhibitors include the uncoupler, carbonyl cyanide p-trifluoromethoxyhydrazone, ADP + Pi, the thiol reagents N-ethylmaleimide and p-hydroxymercuribenzoate and inhibitors of the mitochondrial transport of carboxylic acids. In some cases, the GSH concentration of the mitochondria during the reductions correlates with the reduction rate (e.g. with succinate and after N-ethylmaleimide) but in others it is dissociated. The results suggest that hydroperoxide reduction requires the GSH-glutathione
Ubiquinol is produced normally in cells from Coenzyme Q10 to facilitate the energy transfer from a multitude of fat- and carbohydrate-burning chemical processes to the production of energy in the form of ATP. Ubiquinol deficiency hits the most active organs of the body first, which are the heart, brain and kidneys. Low levels of ubiquinol and CoQ10 occur as people age, or as a side effect of cholesterol-lowering therapy through statin drugs, which diminish the production of CoQ10 in the liver. CoQ10 has a lower potency than ubiquinol active form, because it has less prominent antioxidant properties, although it retains the same energy-enhancing effects. Ubiquinol energy production takes place in special cellular power-plants called mitochondria, where the nutrients we obtain from food are burned and the energy is transferred and carried by CoQ10 and ubiquinol to form more ATP, which is the molecule that releases energy whenever and wherever it is needed. Therefore, ubiquinol active form is ...
Summary is not available for the mouse gene. This summary is for the human ortholog.] This gene encodes a ubiquinone-binding protein of low molecular mass. This protein is a small core-associated protein and a subunit of ubiquinol-cytochrome c reductase complex III, which is part of the mitochondrial respiratory chain. [provided by RefSeq, Jul 2008 ...
UQCC1 - UQCC (untagged)-Human ubiquinol-cytochrome c reductase complex chaperone (UQCC), nuclear gene encoding mitochondrial protein, transcript variant 1 available for purchase from OriGene - Your Gene Company.
Complete information for UQCRBP1 gene (Pseudogene), Ubiquinol-Cytochrome C Reductase Binding Protein Pseudogene 1, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
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|p|The body uses two forms of CoQ10. |I|Ubiquinone|/I|, also known as the oxidized form, is better known and is used primarily for energy production in the electron transport energy cycle inside the cell. |I|Ubiquinol|/I| plays a primary role in decreasin
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As you know, Co Q 10 is a fat-soluble vitamin-like substance found naturally in all forms of animal life. It is biosynthesized in the membranes of cells in humans and is vital in the production of energy. It is found in most cells, with especially high concentration in the heart (the organ that requires high levels of energy for normal operation). If that wasnt enough, its an antioxidant as well.. Co Q10 in your body needs to convert it to Ubiquinol, but as we age, we are less efficient at converting it.. For the first time, a kosher stabilized Ubiquinol is now available with Maxi CO-Q Ubiquinol™, providing 100 mg of high-absorption CoQ10 in a single liquid kosher capsule.. Try Maxi CO Q Ubiquinol™!. ...
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Atta, M.A (2009). "Antimycin-A Antibiotic Biosynthesis Produced by Streptomyces Sp. AZ-AR-262: Taxonomy, Fermentation, ...
... s are antimycin antibiotics isolated from marine actinomycete. Imamura, N.; Nishijima, M.; Adachi, K.; Sano, H. ( ... 1993). "Novel antimycin antibiotics, urauchimycins a and B, produced by marine actinomycete". The Journal of Antibiotics. 46 (2 ...
"Two Antimycin A Analogues from Marine-Derived Actinomycete Streptomyces lusitanus". Marine Drugs. 10 (12): 668-676. doi:10.3390 ...
Examples of piscicides include rotenone, saponins, TFM, niclosamide and Antimycin A (Fintrol). Historically, fishing techniques ...
This complex is inhibited by dimercaprol (British Antilewisite, BAL), Napthoquinone and Antimycin. In complex IV (cytochrome c ... by a high membrane potential or respiratory inhibitors such as antimycin A), Complex III may leak electrons to molecular oxygen ...
When piscides are used, antimycin is often the preferred choice as there is little impact on lake invertebrates and its ... Two of the traditionally used piscidies in lake management are rotenone and antimycin. Chemical applications are often looked ...
As such, standard fish poisons or piscicides (e.g., rotenone and antimycin A) that are transmitted across the gill membrane may ... Serial pesticide dilutions of antimycin-A were tested and found to be innocuous. No changes in morbidity and mortality were ...
Reconstitution of antimycin-insensitive electron transfer with the iron-sulfur protein and cytochrome c1". The Journal of ...
Tappel had the (erroneous) idea that inhibitors like antimycin and alkyl hydroxyquinoline-N-oxide might work by chelating iron ... "Inhibition of electron transport by antimycin A, alkyl hydroxy naphthoquinones and metal coordination compounds". Biochem. ...
The fungus is also susceptible to antimycins produced by Streptomyces species. Conversely, P. fastigiata exhibits antimicrobial ...
Antimycin A - used in fishery management, this compound produces large quantities of this free radical. ...
Smith MJ, Simco BA, Warren CO (December 1975). "Comparative effects of antimycin A on isolated mitochondria of channel catfish ...
Piscicide Change from Antimycin to Rotenone". National Park Service - U.S. Department of the Interior. Retrieved 18 July 2013. ...
The controversy stemmed from the poison antimycin used to kill the other fish in the stream to make way for the trout. In 2008 ...
Electron leakage occurs mainly at the Qo site and is stimulated by antimycin A. Antimycin A locks the b hemes in the reduced ... Antimycin A binds to the Qi site and inhibits the transfer of electrons in Complex III from heme bH to oxidized Q (Qi site ...
An antibiotic, antimycin A, and British anti-Lewisite, an antidote used against chemical weapons, are the two important ...
There are other chemicals that interrupt the mitochondrial electron transport chain (e.g., rotenone, antimycin A) and produce ...
This can be done by poisoning rivers with chemicals such as antimycin or rotenone which have been declared safe in the U.S. by ...
... and introduction of the toxin and inhibitor of cellular respiration antimycin A. They also created small barriers to keep new ...
Antimycin A - compound produced by this bacterium used in piscicides Streptomyces isolates Van der Meij, A., Willemse, J., ...
... is used in biomedical research to study oxygen consumption rate of cells usually in combination with antimycin A (an ...
He showed that the binding of certain inhibitors of oxidative phosphorylation acting at different sites (antimycin on electron ...
Antimony pentafluoride Antimycin A ANTU (Alpha-Naphthylthiourea) Arsenic pentoxide Arsenous oxide Arsenous trichloride Arsine ...
... antimycin a MeSH D04.345.349.100 - brefeldin a MeSH D04.345.349.125 - candicidin MeSH D04.345.349.156 - cytochalasins MeSH ...
Antimycins are produced by a non-ribosomal peptide synthetase (NRPS)/polyketide synthase (PKS) assembly complex which acts as ... Antimycins are produced as secondary metabolites by Streptomyces bacteria, a soil bacteria. These specialized metabolites ... The following steps describe chemically what the Ant Enzymes do in order to synthesize Antimycin. Synthesis begins with ... Seipke, Ryan F; Hutchings, Matthew I (2013). "The regulation and biosynthesis of antimycins". Beilstein Journal of Organic ...
When Antimycin A is added at 25 ppb it provides a complete kill. However at 10 ppb, Antimycin A is used as a selective killing ... Antimycin A (more exactly Antimycin A1b) is a secondary metabolite produced by Streptomyces bacteria and a member of a group of ... Antimycin A is the active ingredient in Fintrol, a chemical piscicide (fish poison) used in fisheries management. Antimycin A ... Antimycin A is an inhibitor of cellular respiration, specifically oxidative phosphorylation. Antimycin A binds to the Qi site ...
Antimycin A Piscicide Complex III Binds to the Qi site of cytochrome c reductase, thereby inhibiting the oxidation of ubiquinol ...
Solvent vehicles are being tested for effective dissolution of the Antimycin A prior to testing its effects with various fish ...
Antimycins are produced by a non-ribosomal peptide synthetase (NRPS)/polyketide synthase (PKS) assembly complex which acts as ... Antimycins are produced as secondary metabolites by Streptomyces bacteria, a soil bacteria. These specialized metabolites ... The following steps describe chemically what the Ant Enzymes do in order to synthesize Antimycin. Synthesis begins with ... Seipke, Ryan F; Hutchings, Matthew I (2013). "The regulation and biosynthesis of antimycins". Beilstein Journal of Organic ...
When Antimycin A is added at 25 ppb it provides a complete kill. However at 10 ppb, Antimycin A is used as a selective killing ... Antimycin A (more exactly Antimycin A1b) is a secondary metabolite produced by Streptomyces bacteria and a member of a group of ... Antimycin A is the active ingredient in Fintrol, a chemical piscicide (fish poison) used in fisheries management. Antimycin A ... Antimycin A is an inhibitor of cellular respiration, specifically oxidative phosphorylation. Antimycin A binds to the Qi site ...
We will also be using a beeswax microparticle to contain the antimycin-A, which will minimize the leaching of antimycin-A into ... If sufficient antimycin-A is not available for use, yttrium will be used as an inert marker to determine if fish consumed the ... For example, a microparticle made of wax will be used to deliver the control chemical, which will most likely be antimycin-A, a ... Determine the leach rate of antimycin-A from the bait, and also determine if the leach rate is sufficient to cause mortality; ...
Antimycin A , C28H40N2O9 , CID 14957 - structure, chemical names, physical and chemical properties, classification, patents, ...
antimycin A1 , C28H40N2O9 , CID 12550 - structure, chemical names, physical and chemical properties, classification, patents, ...
2-Methoxy antimycin reveals a unique mechanism for Bcl-xL inhibition. Pamela S. Schwartz, Michael K. Manion, Christine B. ... 2-Methoxy antimycin reveals a unique mechanism for Bcl-xL inhibition Message Subject (Your Name) has forwarded a page to you ... 2-Methoxy antimycin reveals a unique mechanism for Bcl-xL inhibition ... 2-Methoxy antimycin reveals a unique mechanism for Bcl-xL inhibition ...
2-Methoxy antimycin reveals a unique mechanism for Bcl-xL inhibition. Pamela S. Schwartz, Michael K. Manion, Christine B. ... 2-Methoxy antimycin reveals a unique mechanism for Bcl-xL inhibition Message Subject (Your Name) has forwarded a page to you ... We analyze the selective cytotoxicity of one Bcl-xL inhibitor, 2-methoxy antimycin A, toward cells with excess exogenous Bcl-xL ... Treatment with 2-methoxy antimycin A acutely reverses the metabolic effects of Bcl-xL, causing mitochondrial hyperpolarization ...
Although a base-line resolution of the known four major antimycins Al, A2, A3, and A4 was readily achieved with mobile phases ... a mixture of antimycins A was separated into eight hitherto unreported subcomponents, Ala, Alb, A2a, A2b, A3a, A3b, A4a, and ... Reversed-phase thin-layer chromatography of homologs of Antimycin-A and related derivatives. Journal of Chromatography By:. ... Although a base-line resolution of the known four major antimycins Al, A2, A3, and A4 was readily achieved with mobile phases ...
We used Antimycin-A to induce cell death in myocyte through mitochondrial dysfunction. We then determined the dose and time of ... Quercetin, Antimycin-A and DMSO were obtained from Sigma Chemical Co (St Louis, MO). PenStrep and DMEM medium were obtained ... Quercetin Protects Rat L6 Myocytes from Antimycin A-Induced Mitochondrial Dysfunction Vijay M Kale* College of Pharmacy, ... Antimycin-A (AMA) damages the mitochondria through inhibition of mitochondrial electron transport. The present study sought to ...
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Desiree) were sprayed with antimycin A, an inhibitor of the cytochrome pathway. Enzyme capacities of NAD(P)H dehydrogenases (EC ... We report a specific decrease in internal rotenone-insensitive NADH dehydrogenase capacity in mitochondria from antimycin A- ... The internal rotenone-insensitive NADH oxidation decreases after antimycin A treatment of potato leaves. However, the decrease ... With the 30 μM antimycin A treatment, the rates were completely insensitive to in vitro addition of antimycin A (data not shown ...
In Candida albicans, cyanide and antimycin A inhibited K(+) transport, not only with ethanol-O2 as the substrate, but also with ... MECHANISMS INVOLVED IN THE INHIBITION OF GLYCOLYSIS BY CYANIDE AND ANTIMYCIN A IN CANDIDA ALBICANS AND ITS REVERSAL BY HYDROGEN ... to an activity by which H2O2 can be reduced by electrons flowing from NADH through a pathway that can be inhibited by antimycin ...
How Antimycin Affects the Function of Mitochondria. First, antimycin A binds to the Q site of cytochrome c reductase, ... Antimycin is a mitochondrial inhibitor which is involved in the energy-coupling site of the respiratory system. Antimycin A ... Antimycin Topics: Cellular respiration, Oxidative phosphorylation, Adenosine triphosphate Pages: 3 (648 words) Published: ... Antimycin is now used as a commerical fish toxicant and is the active ingredient in Fintrol, a commerical piscicide used in ...
Antimycin A1 inhibits angiogenesis through decrease in VEGF production caused by inhibition of HIF-1α activation. - Mechanism ... Antimycin A1 is a specific electron transfer inhibitor of ubiquinol-cytochrome c oxidoreductase. ... Antimycin A1642-15-9Antimycin A 1Antimycin A-1Mitochondrial Metabolismmitochondrialbc1complexelectrontransferBcl-xLBcl-2 ... Antimycin A1 is a specific electron transfer inhibitor of ubiquinol-cytochrome c oxidoreductase. Antimycin A1 inhibits ...
The two best-known antimycins are antimycin A1 ({C28H40N2O9}) and antimycin A3 ({C26H36N2O9}). They are notable for their ... antimycin. antimycin an`ti*my"cin ([a^]n`t[i^]*m[imac]"s[i^]n), n. 1. one of several antibiotic substances produced by several ... Antimycin A - Chembox new ImageFile=Antimycin A.svg ImageSize= IUPACName= (2{R},3(S},6{S},7{R},8{R}) 3 [(3 formamido 2 ... Antimycin - steht für: Antimycin A, einen Hemmstoff des Komplex III der Atmungskette. Citrinin, ein Mykotoxin. Diese Seite ist ...
Antimycin A CAS Type 1 Name Butanoic acid, 2(or 3)-methyl-, 3-((3-(formylamino)-2-hydroxybenzoyl)amino)-8-hexyl-2,6-dimethyl-4, ... Antimycin A1 has been used as a fungicide, insecticide, and miticide. (From Merck Index, 12th ed). ...
Antimycin A1 is soluble in ethanol, methanol, DMF and DMSO.. Mechanism of Action. Antimycin A1 inhibits angiogenesis via a ... Antimycin A1 is the most hydrophobic of the four analogues of the antimycin A complex. Although broadly active as respiration ... Antimycin A1, an antibiotic with insecticidal and miticidal properties. Kido G.S. & Spyhalski E. Science 1950, 112, 172.. ... Inhibition of angiogenesis and HIF-1a activity by antimycin A1. Maeda M. et al. Biol. Pharm. Bull. 2006, 29, 1344. ...
Antimycin A, Contain 100mg. Brand. SIGMA-ALDRICH. Item #. 45ZE33. Mfr. Model #. A8674-100MG ...
Antimycin A3 is a potent inhibitor of respiration. Antimycin A3 inhibits the electron transfer activity of ubiquinol-cytochrome ... Antimycin A3 inhibits ATP-citrate lyase with a Ki value of 60.1 µM. - Mechanism of Action & Protocol. ... Antimycin A3, an antibiotic isolated from a number of Streptomyces species, shows antifungal activities. ... Antimycin A3Antimycin A 3Antimycin A-3Mitochondrial MetabolismapoptosisBcl-2Bcl-XLelectrontransferubiquinol-cytochromec ...
Antimycin A-insensitive oxidation of NADPH, NADH and succinate was measured to oxygen in the presence of DTT and pyruvate to ... With the 30 μM antimycin A treatment, the rates were completely insensitive to in vitro addition of antimycin A (data not shown ... With the 30 μM antimycin A treatment, the rates were completely insensitive to in vitro addition of antimycin A (data not shown ... Antimycin A-insensitive oxidation of NADPH, NADH and succinate was measured to oxygen in the presence of DTT and pyruvate to ...
A New Antibiotic, Antimycin A9, Produced by Streptomyces sp. K01-0031 *Kazuro Shiomi ... Rights & permissionsfor article A New Antibiotic, Antimycin A,sub,9,/sub,, Produced by ,i,Streptomyces,/i, sp. K01-0031 . Opens ...
Almeida, E. L., Margassery, L. M., Kennedy, J. and Dobson, A. D. W. (2018) Draft genome sequence of the antimycin-producing ... Draft genome sequence of the antimycin-producing bacterium Streptomyces sp. strain SM8, isolated from the marine sponge ... Draft genome sequence of the antimycin-producing bacterium Streptomyces sp. strain SM8, isolated from the marine sponge ...
A marked age-dependent response was observed with 2-deoxyglucose but not with antimycin A. The results confirm an increase in ... The relative growth inhibitory effects of 2-deoxyglucose and antimycin A were monitored at five stages during the life-span in ... The relative growth inhibitory effects of 2-deoxyglucose and antimycin A were monitored at five stages during the life-span in ... A marked age-dependent response was observed with 2-deoxyglucose but not with antimycin A. The results confirm an increase in ...
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Genetic Evidence for Cytochrome b Qi Site Inhibition by 4(1H)-quinolone-3-diarylethers and Antimycin in Toxoplasma gondii ... to possess a Thr222-Pro amino acid substitution that confers 49-fold resistance to ELQ-316 and 19-fold resistance to antimycin ...
H2O2 Activates the Antimycin A-Insensitive Pathway.. H2O2-induced CEF was insensitive to antimycin A (Fig. 2B). In addition, ... Infiltration with 20 μM antimycin A was carried out in darkness for 3 h. Successful antimycin A infiltration was confirmed by ... 2B, ANCOVA, P , 0.05, n = 3), well above the observed Ki for inhibition of the antimycin A-sensitive pathway of CEF (51). These ... Infiltration of Leaves with H2O2, Methyl Viologen, and Antimycin A.. To determine the effects of H2O2 on CEF, Col-0 leaves were ...
Reprogramming of the antimycin NRPS-PKS assembly lines inspired by gene evolution Modifying the non-ribosomal peptide synthase ...
Antimycins (,40 members) were discovered nearly 65 years ago but the discovery of the gene cluster encoding antimycin ... antimycins,gene regulation,genome mining,natural products,streptomyces. Faculty \ School:. Faculty of Science , School of ... Antimycin A is widely used as a piscicide in the catfish farming industry and also has potent killing activity against insects ... However, more recently, antimycin A has attracted attention as a potent and selective inhibitor of the mitochondrial anti- ...
Crystal Structure of Mitochondrial Cytochrome bc1 in Complex with Antimycin A1. *DOI: 10.2210/pdb1ntk/pdb ...
  • Antimycin A is an inhibitor of cellular respiration, specifically oxidative phosphorylation. (wikipedia.org)
  • We analyze the selective cytotoxicity of one Bcl-x L inhibitor, 2-methoxy antimycin A, toward cells with excess exogenous Bcl-x L in isogenic cell line pairs. (aacrjournals.org)
  • Treatment with 2-methoxy antimycin A acutely reverses the metabolic effects of Bcl-x L , causing mitochondrial hyperpolarization and a progressive increase in mitochondrial NAD(P)H. We identify an additional small-molecule Bcl-x L inhibitor, NSC 310343, establishing a class of Bcl-x L inhibitors with gain-of-function activity. (aacrjournals.org)
  • Desiree) were sprayed with antimycin A, an inhibitor of the cytochrome pathway. (biomedcentral.com)
  • Several reports describe an induction of the alternative pathway by treatment with antimycin A, an inhibitor of the bc 1 complex. (biomedcentral.com)
  • Antimycin is a mitochondrial inhibitor which is involved in the energy-coupling site of the respiratory system. (studymode.com)
  • Antimycin A1 is a specific electron transfer inhibitor of ubiquinol-cytochrome c oxidoreductase . (medchemexpress.com)
  • Antimycin A3 is a potent inhibitor of respiration . (medchemexpress.com)
  • A T. gondii strain selected under ELQ-316 drug pressure was found to possess a Thr222-Pro amino acid substitution that confers 49-fold resistance to ELQ-316 and 19-fold resistance to antimycin, a well-characterized Qi site inhibitor. (blogspot.com)
  • However, more recently, antimycin A has attracted attention as a potent and selective inhibitor of the mitochondrial anti-apoptotic proteins Bcl-2 and Bcl-xL. (uea.ac.uk)
  • Conclusion: This studies demonstrated that the opened-chain analogues of antimycin A 3 , AMD2 and AMD4 as a promising candidates of caspase inhibitor of apoptosis in CRC. (ui.ac.id)
  • Extensive binding interactions and conformational adjustments of residues lining the Q(i) pocket provide a structural basis for the high affinity binding of antimycin A and for phenotypes of inhibitor resistance. (rcsb.org)
  • 5 m l of 0.5M G3P (effective 5mM) and 5 m l of 2 m M Antimycin (20nM final) are added as substrate and inhibitor respectively after the inhibition of complexes I and II. (mitomap.org)
  • Antimycin A (AA), a mitochondrial electron transport chain inhibitor, and monofluroacetate (MFA), a TCA cycle inhibitor, induced expression of the transgene and the endogenous gene in parallel. (deepdyve.com)
  • Among the respiratory chain inhibitors, ROS generation could be effectively eliminated with myxothiazol, which inhibits oxidation of ubiquinol to the ubisemiquinone radical by the Rieske iron-sulfur center of complex III, but not with antimycin A, an inhibitor of electron transport that is functional in further oxidation of the ubisemiquinone radical to ubiquinone in the Q cycle of complex III. (asm.org)
  • Although a base-line resolution of the known four major antimycins Al, A2, A3, and A4 was readily achieved with mobile phases containing acetate buffers, the separation of the new antibiotic subcomponents was highly sensitive to variation in mobile phase conditions. (usgs.gov)
  • Antimycin A is an antibiotic substance produced by Streptomyces bacteria. (studymode.com)
  • antimycin A - an·ti·my·cin A .ant i .mīs ən ā n a crystalline antibiotic C28H40N2O9 used esp. (academic.ru)
  • Antimycin A1, an antibiotic with insecticidal and miticidal properties. (toku-e.com)
  • Antimycin A3, an antibiotic isolated from a number of Streptomyces species, shows antifungal activities. (medchemexpress.com)
  • A New Antibiotic, Antimycin A 9 , Produced by Streptomyces sp. (nature.com)
  • We report a specific decrease in internal rotenone-insensitive NADH dehydrogenase capacity in mitochondria from antimycin A-treated leaves. (biomedcentral.com)
  • The internal rotenone-insensitive NADH oxidation decreases after antimycin A treatment of potato leaves.However, the decrease is not due to changes in expression of known nda genes.One consequence of the lower NADH dehydrogenase capacity may be a stabilisation of the respiratory chain reduction level, should the overall capacity of the cytochrome and the alternative pathway be restricted. (nih.gov)
  • Treatment with rotenone or antimycin A also resulted in increased wortmannin-sensitive Akt phosphorylation, probably by increasing intracellular H2O2 generation by blocking mitochondrial electron transport. (nih.gov)
  • Insulin release was mimicked by the mitochondrial-complex blockers, antimycin and rotenone, that generate mROS. (diabetesjournals.org)
  • The inhibitors rotenone and antimycin are very powerful and tend to stick to the glass chamber, membrane and syringes. (mitomap.org)
  • With the 30 μM antimycin A treatment, the rates were completely insensitive to in vitro addition of antimycin A (data not shown), indicating a high degree of in vivo bc1 complex inhibition at this concentration. (nih.gov)
  • Differential growth inhibition of human diploid fibroblasts by 2-deoxyglucose and antimycin A with ageing in vitro. (semanticscholar.org)
  • The relative growth inhibitory effects of 2-deoxyglucose and antimycin A were monitored at five stages during the life-span in vitro of human diploid fibroblasts. (semanticscholar.org)
  • No difference in AOX capacity is seen between mitochondria from antimycin A-treated leaves and control leaves. (nih.gov)
  • Antimycins, inhibitors of ATP-citrate lyase, from a Streptomyces sp. (medchemexpress.com)
  • Objective: Studies of open-chain analogues of antimycin A 3 as caspase inhibitors of apoptosis by molecular docking approach through computeraided drug design. (ui.ac.id)
  • Antimycin-A (AMA) damages the mitochondria through inhibition of mitochondrial electron transport. (omicsonline.org)
  • Mechanisms involved in the inhibition of glycolysis by cyanide and antimycin A in Candida albicans and its reversal by hydrogen peroxide. (unam.mx)
  • Antimycin A1 inhibits angiogenesis through decrease in VEGF production caused by inhibition of HIF-1α activation. (medchemexpress.com)
  • Inhibition of angiogenesis and HIF-1alpha activity by antimycin A1. (medchemexpress.com)
  • Inhibition of electron transport of rat liver mitochondria by unnatural (-)-antimycin A3. (medchemexpress.com)
  • Remarkably, this inhibition is independent of the main mode of action of antimycins such that an artificial derivative named 2-methoxyantimycin A inhibits Bcl-xL but does not inhibit respiration. (uea.ac.uk)
  • Researchers found that the toxic effects of antimycin were a result of their inhibitory effects on mitochondrial respiration, which disrupt and impair metabolic pathways. (studymode.com)
  • The mode of action of antimycins is to inhibit cytochrome c reductase in the electron transport chain and halt respiration. (uea.ac.uk)
  • Antimycin A is used in research models to study mitochondrial respiration and superoxide production. (thomassci.com)
  • First, antimycin A binds to the Q site of cytochrome c reductase, inhibiting the oxidation of ubiquinol in the electron transport chain of oxidative phosphorylation. (studymode.com)
  • Antimycin A binds cytochrome c reductase, inhibiting electron transport chain activity, oxidative phosphorylation, and ATP synthesis. (thomassci.com)
  • Antimycin A3 inhibits the electron transfer activity of ubiquinol-cytochrome c oxidoreductase . (medchemexpress.com)
  • Antimycin A (AMA) damages mitochondria by inhibiting mitochondrial electron transport and can produce reactive oxygen species (ROS). (omictools.com)
  • Antimycin A inhibits Bcl-2 and Bcl-xL proteins, inducing apoptosis [4] . (medchemexpress.com)
  • Liu J, et al, Biosynthesis of antimycins with a reconstituted 3-formamidosalicylate pharmacophore in Escherichia coli. (medchemexpress.com)
  • 40 members) were discovered nearly 65 years ago but the discovery of the gene cluster encoding antimycin biosynthesis in 2011 has facilitated rapid progress in understanding the unusual biosynthetic pathway. (uea.ac.uk)
  • Antimycin A (more exactly Antimycin A1b) is a secondary metabolite produced by Streptomyces bacteria and a member of a group of related compounds called antimycins. (wikipedia.org)
  • antimycin A - a chemical produced by streptomyces bacteria and used in a commercial preparation as a piscicide, e.g. in the catfish industry. (academic.ru)
  • The antifungal antimycins are not only active against pathogenic fungi but also the garden fungus L. gongylophorus itself. (pnas.org)
  • Antimycin A binds to the Qi site of cytochrome c reductase, inhibiting the oxidation of ubiquinone in the Qi site of ubiquinol thereby disrupting the Q-cycle of enzyme turn over. (wikipedia.org)
  • Because Antimycin A binds to a specific protein in the electron transport chain, its toxicity can be highly species dependent because of subtle species specific differences in ubiquinol. (wikipedia.org)
  • Antimycin A is the active ingredient in Fintrol, a chemical piscicide (fish poison) used in fisheries management. (wikipedia.org)
  • For example, a microparticle made of wax will be used to deliver the control chemical, which will most likely be antimycin-A, a registered piscicide. (usgs.gov)
  • Antimycin is now used as a commerical fish toxicant and is the active ingredient in Fintrol, a commerical piscicide used in fisheries management and in the catfish industry. (studymode.com)
  • Antimycin A is widely used as a piscicide in the catfish farming industry and also has potent killing activity against insects, nematodes and fungi. (uea.ac.uk)
  • The cyanide effect could be reversed by hydrogen peroxide, mainly due to an activity by which H2O2 can be reduced by electrons flowing from NADH through a pathway that can be inhibited by antimycin A, and appears to be a cytochrome c peroxidase. (unam.mx)
  • Although cyanide acts to block the electron transport chain, Antimycin A and cyanide act in different mechanisms. (wikipedia.org)
  • In Candida albicans, cyanide and antimycin A inhibited K(+) transport, not only with ethanol-O2 as the substrate, but also with glucose. (unam.mx)
  • Antimycin A (1 microM) and potassium cyanide (KCN, 100 microM) paralyzed B. pahangi incubated in 10 mM glutamine, an effect antagonized by glucose. (biomedsearch.com)
  • Antimycin A1 is the most hydrophobic of the four analogues of the antimycin A complex. (toku-e.com)
  • The novelty of this study is finding the potential antimycin A 3 analogues which structurally modified against caspases. (ui.ac.id)
  • Analogues of antimycin A 3 as lead compounds were designed and assessed using Molsoft drug-likeness. (ui.ac.id)
  • Results: Analogues of antimycin A 3 has been done by evaluating their physicochemical properties as lead compounds. (ui.ac.id)
  • A marked age-dependent response was observed with 2-deoxyglucose but not with antimycin A. The results confirm an increase in the rate of glycolysis with ageing, which appears to be independent of cellular mitochondrial respiratory chain capacity. (semanticscholar.org)
  • In deeper bodies of water, a pump mechanism is used to disperse Antimycin A through a perforated hose stretching the length of the water column. (wikipedia.org)
  • This enzyme bypasses the proton-pumping cytochrome pathway, consisting of the antimycin A-sensitive bc 1 complex (EC 1.10.2.2) and the cytochrome c oxidase (EC 1.9.3.1). (biomedcentral.com)
  • To determine the capacity of the AOX, the cytochrome pathway activity was completely inhibited by adding antimycin A to the reaction medium. (nih.gov)
  • Antimycins are produced as secondary metabolites by Streptomyces bacteria, a soil bacteria. (wikipedia.org)
  • Fungus-growing attine ants have been shown to use antimycins - produced by symbiotic Streptomyces bacteria - in their fungiculture, to inhibit non-cultivar (i.e. pathogenic) fungi. (wikipedia.org)
  • One research group studying these symbiotic Streptomyces bacteria recently identified the biosynthetic gene cluster for antimycins, which was unknown despite the compounds themselves being identified 60 years ago. (wikipedia.org)
  • Bernardy J.A., Hubert T.D., Ogorek J.M. & Schmidt L.J. (2013) Determination of Antimycin-A in Water by Liquid Chromatographic/Mass Spectrometry: Single-Laboratory Validation. (usgs.gov)
  • Antimycin A-insensitive oxidation of NADPH, NADH and succinate was measured to oxygen in the presence of DTT and pyruvate to assure maximum rates. (nih.gov)
  • Effects of quercetin on Antimycin-A induced mitochondrial dysfunction was studied using cytotoxicity, ATP levels, mitochondrial superoxide production and NDUFB8 mRNA expression. (omicsonline.org)
  • Draft genome sequence of the antimycin-producing bacterium Streptomyces sp. (ucc.ie)
  • Antimycins are produced by a non-ribosomal peptide synthetase (NRPS)/polyketide synthase (PKS) assembly complex which acts as an assembly line for antimycin production. (wikipedia.org)
  • The [ rho 0 ] mutants and antimycin-treated cells differ from the wild type in PPM composition and invertase, acid phosphatase, and glucoamylase activities. (asm.org)
  • Antimycin A3 induces apoptosis of cancer cells by selectively killing cancer cells that expressed high levels of anti-apoptotic Bcl-2 and Bcl-XL [1] . (medchemexpress.com)
  • The Bcl-2/Bcl-xL family of proteins are over-produced in cancer cells that are resistant to apoptosis-inducing chemotherapy agents, so antimycins have great potential as anticancer drugs used in combination with existing chemotherapeutics. (uea.ac.uk)
  • To generate ROS, we applied antimycin A to explant cultures of auditory epithelia, and examined the effect of hydrogen on the protection of hair cells against ROS. (nih.gov)
  • Ligands implicated in flocculation of mutants or antimycin-treated cells were not aggregated as much by concanavalin A as were those of the wild type. (asm.org)
  • The reduced flocculation of cells grown in the presence of antimycin, under anaerobiosis, or carrying a [ rho 0 ] mutation may be the consequence of alterations of PPM structures which are the ligands of lectins, both involved in this cell-cell recognition phenomenon. (asm.org)
  • The movement of nucleophosmin from nucleoli to nucleoplasm in HeLa cells induced by cytotoxic drugs and detected by immunofluorescence is inhibited by concomitant treatment with antimycin A in glucose-free medium. (biomedsearch.com)
  • Synthesis and anticancer activity of polyhydroxylated 18-membered analogue of antimycin A3. (medchemexpress.com)
  • Several secondary metabolite biosynthetic gene clusters are present, encoding known and novel metabolites, including antimycin. (ucc.ie)
  • Here we review what is known about antimycins, the regulation of the ant gene cluster and the unusual biosynthetic pathway. (uea.ac.uk)
  • H 2 O 2 -dependent CEF was not sensitive to antimycin A or loss of PGR5, indicating that increased CEF probably does not involve the PGR5-PGRL1 associated pathway. (pnas.org)
  • rao7/myb29 mutants have increased levels of AOX1a transcript and protein compared to wild type after induction with antimycin A. A variety of genes previously associated with the mitochondrial stress response also display enhanced transcript abundance, indicating that RAO7/MYB29 negatively regulates mitochondrial stress responses in general. (plantphysiol.org)
  • Solvent vehicles are being tested for effective dissolution of the Antimycin A prior to testing its effects with various fish species' blood. (usgs.gov)
  • In aquaculture, Antimycin A is used as an agent to enhance catfish production via selective killing small and more sensitive species. (wikipedia.org)
  • However at 10 ppb, Antimycin A is used as a selective killing agent to kill smaller or more sensitive species that may reduce the yield of commercial farming. (wikipedia.org)
  • We will also be using a beeswax microparticle to contain the antimycin-A, which will minimize the leaching of antimycin-A into the water and increase species specificity simultaneously. (usgs.gov)
  • Antimycin A1 has been used as a fungicide, insecticide, and miticide. (ctdbase.org)
  • The highest levels of cox1, cox3, and cob transcripts were observed in 4 h and atp9 transcripts in 6 h after treatment with antimycin A (antA). (deepdyve.com)
  • The structures of bovine mitochondrial bc(1) in the presence or absence of bound substrate ubiquinone and with either the bound antimycin A(1) or NQNO were determined and refined. (rcsb.org)