Bongkrekic Acid: An antibiotic produced by Pseudomonas cocovenenans. It is an inhibitor of MITOCHONDRIAL ADP, ATP TRANSLOCASES. Specifically, it blocks adenine nucleotide efflux from mitochondria by enhancing membrane binding.Atractyloside: A glycoside of a kaurene type diterpene that is found in some plants including Atractylis gummifera (ATRACTYLIS); COFFEE; XANTHIUM, and CALLILEPIS. Toxicity is due to inhibition of ADENINE NUCLEOTIDE TRANSLOCASE.Mitochondrial ADP, ATP Translocases: A class of nucleotide translocases found abundantly in mitochondria that function as integral components of the inner mitochondrial membrane. They facilitate the exchange of ADP and ATP between the cytosol and the mitochondria, thereby linking the subcellular compartments of ATP production to those of ATP utilization.Burkholderia gladioli: A species of gram-negative, aerobic bacteria that acts as both a human and plant pathogen.Mitochondria: 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)Mitochondrial Swelling: An increase in MITOCHONDRIAL VOLUME due to an influx of fluid; it occurs in hypotonic solutions due to osmotic pressure and in isotonic solutions as a result of altered permeability of the membranes of respiring mitochondria.Mitochondrial Membrane Transport Proteins: Proteins involved in the transport of specific substances across the membranes of the MITOCHONDRIA.Oligomycins: 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).Intracellular Membranes: Thin structures that encapsulate subcellular structures or ORGANELLES in EUKARYOTIC CELLS. They include a variety of membranes associated with the CELL NUCLEUS; the MITOCHONDRIA; the GOLGI APPARATUS; the ENDOPLASMIC RETICULUM; LYSOSOMES; PLASTIDS; and VACUOLES.Permeability: Property of membranes and other structures to permit passage of light, heat, gases, liquids, metabolites, and mineral ions.Cyclosporine: A cyclic undecapeptide from an extract of soil fungi. It is a powerful immunosupressant with a specific action on T-lymphocytes. It is used for the prophylaxis of graft rejection in organ and tissue transplantation. (From Martindale, The Extra Pharmacopoeia, 30th ed).Caspase 9: A long pro-domain caspase that contains a caspase recruitment domain in its pro-domain region. Caspase 9 is activated during cell stress by mitochondria-derived proapoptotic factors and by CARD SIGNALING ADAPTOR PROTEINS such as APOPTOTIC PROTEASE-ACTIVATING FACTOR 1. It activates APOPTOSIS by cleaving and activating EFFECTOR CASPASES.Cytochrome c Group: 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)Membrane Potentials: The voltage differences across a membrane. For cellular membranes they are computed by subtracting the voltage measured outside the membrane from the voltage measured inside the membrane. They result from differences of inside versus outside concentration of potassium, sodium, chloride, and other ions across cells' or ORGANELLES membranes. For excitable cells, the resting membrane potentials range between -30 and -100 millivolts. Physical, chemical, or electrical stimuli can make a membrane potential more negative (hyperpolarization), or less negative (depolarization).Apoptosis: One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.Caspases: A family of intracellular CYSTEINE ENDOPEPTIDASES that play a role in regulating INFLAMMATION and APOPTOSIS. They specifically cleave peptides at a CYSTEINE amino acid that follows an ASPARTIC ACID residue. Caspases are activated by proteolytic cleavage of a precursor form to yield large and small subunits that form the enzyme. Since the cleavage site within precursors matches the specificity of caspases, sequential activation of precursors by activated caspases can occur.Adenosine Triphosphate: 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.Mitochondria, Liver: 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)Adenosine Diphosphate: Adenosine 5'-(trihydrogen diphosphate). An adenine nucleotide containing two phosphate groups esterified to the sugar moiety at the 5'-position.Caspase 3: A short pro-domain caspase that plays an effector role in APOPTOSIS. It is activated by INITIATOR CASPASES such as CASPASE 9. Isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.Proto-Oncogene Proteins c-bcl-2: Membrane proteins encoded by the BCL-2 GENES and serving as potent inhibitors of cell death by APOPTOSIS. The proteins are found on mitochondrial, microsomal, and NUCLEAR MEMBRANE sites within many cell types. Overexpression of bcl-2 proteins, due to a translocation of the gene, is associated with follicular lymphoma.Electronic Mail: Messages between computer users via COMPUTER COMMUNICATION NETWORKS. This feature duplicates most of the features of paper mail, such as forwarding, multiple copies, and attachments of images and other file types, but with a speed advantage. The term also refers to an individual message sent in this way.Thyroxine: The major hormone derived from the thyroid gland. Thyroxine is synthesized via the iodination of tyrosines (MONOIODOTYROSINE) and the coupling of iodotyrosines (DIIODOTYROSINE) in the THYROGLOBULIN. Thyroxine is released from thyroglobulin by proteolysis and secreted into the blood. Thyroxine is peripherally deiodinated to form TRIIODOTHYRONINE which exerts a broad spectrum of stimulatory effects on cell metabolism.Adenine NucleotidesAdenine: A purine base and a fundamental unit of ADENINE NUCLEOTIDES.Adenine Nucleotide Translocator 1: A subtype of mitochondrial ADP, ATP translocase found primarily in heart muscle (MYOCARDIUM) and skeletal muscle (MUSCLE, SKELETAL).Reactive Nitrogen Species: Nitrogenous products of NITRIC OXIDE synthases, ranging from NITRIC OXIDE to NITRATES. These reactive nitrogen intermediates also include the inorganic PEROXYNITROUS ACID and the organic S-NITROSOTHIOLS.Fluoresceins: A family of spiro(isobenzofuran-1(3H),9'-(9H)xanthen)-3-one derivatives. These are used as dyes, as indicators for various metals, and as fluorescent labels in immunoassays.Reactive Oxygen Species: 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.Calbindins: Calcium-binding proteins that are found in DISTAL KIDNEY TUBULES, INTESTINES, BRAIN, and other tissues where they bind, buffer and transport cytoplasmic calcium. Calbindins possess a variable number of EF-HAND MOTIFS which contain calcium-binding sites. Some isoforms are regulated by VITAMIN D.Calbindin 1: A calcium-binding protein that mediates calcium HOMEOSTASIS in KIDNEYS, BRAIN, and other tissues. It is found in well-defined populations of NEURONS and is involved in CALCIUM SIGNALING and NEURONAL PLASTICITY. It is regulated in some tissues by VITAMIN D.S100 Calcium Binding Protein G: A calbindin protein found in many mammalian tissues, including the UTERUS, PLACENTA, BONE, PITUITARY GLAND, and KIDNEYS. In intestinal ENTEROCYTES it mediates intracellular calcium transport from apical to basolateral membranes via calcium binding at two EF-HAND MOTIFS. Expression is regulated in some tissues by VITAMIN D.Isothiocyanates: Organic compounds with the general formula R-NCS.Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.Cytochromes c: Cytochromes of the c type that are found in eukaryotic MITOCHONDRIA. They serve as redox intermediates that accept electrons from MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX III and transfer them to MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX IV.Anticarcinogenic Agents: Agents that reduce the frequency or rate of spontaneous or induced tumors independently of the mechanism involved.Metalloendopeptidases: ENDOPEPTIDASES which use a metal such as ZINC in the catalytic mechanism.Matrix Metalloproteinases: A family of zinc-dependent metalloendopeptidases that is involved in the degradation of EXTRACELLULAR MATRIX components.Matrix Metalloproteinase 2: A secreted endopeptidase homologous with INTERSTITIAL COLLAGENASE, but which possesses an additional fibronectin-like domain.Matrix Metalloproteinase Inhibitors: Compounds that inhibit the enzyme activity or activation of MATRIX METALLOPROTEINASES.Matrix Metalloproteinase 9: An endopeptidase that is structurally similar to MATRIX METALLOPROTEINASE 2. It degrades GELATIN types I and V; COLLAGEN TYPE IV; and COLLAGEN TYPE V.Metalloproteases: Proteases which use a metal, normally ZINC, in the catalytic mechanism. This group of enzymes is inactivated by metal CHELATORS.Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere.Artemia: A genus of CRUSTACEA of the order ANOSTRACA, found in briny pools and lakes and often cultured for fish food. It has 168 chromosomes and differs from most crustaceans in that its blood contains hemoglobin.Biology: One of the BIOLOGICAL SCIENCE DISCIPLINES concerned with the origin, structure, development, growth, function, genetics, and reproduction of animals, plants, and microorganisms.Freeze Drying: Method of tissue preparation in which the tissue specimen is frozen and then dehydrated at low temperature in a high vacuum. This method is also used for dehydrating pharmaceutical and food products.Hermaphroditic Organisms: Animals and plants which have, as their normal mode of reproduction, both male and female sex organs in the same individual.Cyclophilins: A family of peptidyl-prolyl cis-trans isomerases that bind to CYCLOSPORINS and regulate the IMMUNE SYSTEM. EC 5.2.1.-Alkynes: Hydrocarbons with at least one triple bond in the linear portion, of the general formula Cn-H2n-2.Adenosine: A nucleoside that is composed of ADENINE and D-RIBOSE. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter.Mersalyl: A toxic thiol mercury salt formerly used as a diuretic. It inhibits various biochemical functions, especially in mitochondria, and is used to study those functions.Organomercury Compounds: Organic compounds which contain mercury as an integral part of the molecule.Ruthenium Red: An inorganic dye used in microscopy for differential staining and as a diagnostic reagent. In research this compound is used to study changes in cytoplasmic concentrations of calcium. Ruthenium red inhibits calcium transport through membrane channels.Thyroid Hormones: Natural hormones secreted by the THYROID GLAND, such as THYROXINE, and their synthetic analogs.Sulfhydryl Reagents: Chemical agents that react with SH groups. This is a chemically diverse group that is used for a variety of purposes. Among these are enzyme inhibition, enzyme reactivation or protection, and labelling.Mitochondria, Heart: The mitochondria of the myocardium.
Induction of apoptosis by valinomycin: mitochondrial permeability transition causes intracellular acidification. (1/100)In order to determine whether disruption of mitochondrial function could trigger apoptosis in murine haematopoietic cells, we used the potassium ionophore valinomycin. Valinomycin induces apoptosis in the murine pre-B cell line BAF3, which cannot be inhibited by interleukin-3 addition or Bcl-2 over-expression. Valinomycin triggers rapid loss of mitochondrial membrane potential. This precedes cytoplasmic acidification, which leads to cysteine-active-site protease activation, DNA fragmentation and cell death. Bongkrekic acid, an inhibitor of the mitochondrial permeability transition, prevents acidification and subsequent induction of apoptosis by valinomycin. (+info)
Death signals from the B cell antigen receptor target mitochondria, activating necrotic and apoptotic death cascades in a murine B cell line, WEHI-231. (2/100)B cell antigen receptor (BCR)-mediated cell death has been proposed as a mechanism for purging the immune repertoire of anti-self specificities during B cell differentiation in bone marrow. Mitochondrial alterations and activation of caspases are required for certain aspects of apoptotic cell death, but how the mitochondria and caspases contribute to BCR-mediated cell death is not well understood. In the present study, we used the mouse WEHI-231 B cell line to demonstrate that mitochondrial alterations and activation of caspases are indeed participants in BCR-mediated cell death. The peptide inhibitor of caspases, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk), blocked cleavage of poly(ADP-ribose) polymerase and various manifestation of nuclear apoptosis such as nuclear fragmentation, hypodiploidy and DNA fragmentation, indicating that signals from the BCR induced the activation of caspases. In addition, z-VAD-fmk delayed apoptosis-associated changes in cellular reduction-oxidation potentials as determined by hypergeneration of superoxide anion, as well as exposure of phosphatidylserine residues in the outer plasma membrane. By contrast, although z-VAD-fmk retarded cytolysis, it was incapable of preventing disruption of the plasma membrane even under the same condition in which it completely blocked nuclear apoptosis. Mitochondrial membrane potential loss was also not blocked by z-VAD-fmk. Bongkrekic acid, a specific inhibitor of mitochondrial permeability transition pores, suppressed not only the mitochondrial membrane potential but also the change of plasma membrane permeability. Overexpression of Bcl-xL prevented mitochondrial dysfunction, nuclear apoptosis and membrane permeability cell death triggered by BCR signal transduction. These observations indicate that death signals from BCR may first cause mitochondrial alterations followed by activation of both necrotic and apoptotic cascades. (+info)
Over-expression of Bcl-2 does not protect cells from hypericin photo-induced mitochondrial membrane depolarization, but delays subsequent events in the apoptotic pathway. (3/100)Hypericin (HY) is a powerful photo-inducer of apoptosis in Jurkat cells as measured by caspase-3 activation, cell shrinkage, phosphatidylserine (PS) exposure and the appearance of hypoploid DNA. These processes are preceded by rapid Bcl-2-independent mitochondrial transmembrane depolarization and a drop in cytoplasmic pH. Pre-incubation of cells with inhibitors of the mitochondrial permeability transition pore, such as cyclosporin A or bongkrekic acid, does not protect cells from mitochondrial membrane potential (deltapsim) decrease. However, monitoring of mitochondrial entrapped calcein by confocal fluorescence imaging gives clear evidence of HY photo-induced mitochondrial permeability. This should be considered as the result of a non-specific alteration of mitochondrial membrane integrity brought about by lipid peroxidation. Nevertheless, synthesis of the anti-apoptotic protein Bcl-2 appears to delay the subsequent time course of PS exposure and to reduce caspase-3 activation and the fraction of cells which become hypoploid. We interpret this partially protective effect as the consequence of a direct interaction of Bcl-2 with cytosolic cytochrome c previously released from mitochondria upon deltapsim decrease and/or of Bcl-2 inhibition of the deleterious retro-effect of caspase-3 on the mitochondrial permeability transition pore and/or the mitochondrial membrane components. (+info)
Antibody evidence for different conformational states of ADP, ATP translocator protein isolated from mitochondria. (4/100)Consistent with the previously proposed reorientation mechanism for the ADP,ATP translocator protein of mitochondria, evidence has now been obtained for the existence of two distinct conformational states of the isolated translocator protein. Previous studies indicated that when the mitochondrial translocator protein is in the c-state(i.e., when its binding site faces the cytosol side) the protein binds primarily the ligand carboxyatractylate (CAT), and when the translocator protein is in the m-state(i.e., when its binding site faces the mitochondrial matrix) the translocator protein binds primarily bongkrekate. Direct evidence for this formulation has now come from the application of antibodies to the isolated translocator protein-ligand complex. Two antibodies were produced against the ADP,ATP translocator protein isolated from beef heart mitochondria. One antibody, which was produced against the protein isolated as the CAT-binding protein complex, was found to be highly specific for that complex and did not react with the protein in the conformation state conferred by the bongkrekate ligand. This antibody did not cover the CAT-binding site, as evidenced by the exchange of unlabeled CAT with [35S]CAT bound to the translocator protein. However, the same antibody inhibited a transition of the protein from the c-state to the m-state, as evidenced by an inhibition of the displacement of[35S]CAT by bongkrekate (added jointly with ADP). It appears, therefore, that the antibody immobilized the translocator protein in the c-state. The second antibody produced against the (somewhat less pure) ADP,ATP translocator protein, isolated as the bongkrekate-binding protein complex, did not react with the CAT-binding protein. Thus, the second antibody appeared to be specific for the translocator protein in the m-state. Neither antibody inhibited mitochondrial ADP,ATP transport. (+info)
Mitochondrial and extramitochondrial apoptotic signaling pathways in cerebrocortical neurons. (5/100)In cultured cerebrocortical neurons, mild excitotoxic insults or staurosporine result in apoptosis. We show here that N-methyl-d-aspartate (NMDA) receptor-mediated, but not staurosporine-mediated, apoptosis is preceded by depolarization of the mitochondrial membrane potential (Deltapsi(m)) and ATP loss. Both insults, however, release cytochrome c (Cyt c) into the cytoplasm. What prompts mitochondria to release Cyt c and the mechanism of release are as yet unknown. We examined the effect of inhibition of the adenine nucleotide translocator (ANT), a putative component of the mitochondrial permeability transition pore. Inhibition of the mitochondrial ANT with bongkrekic acid (BA) prevented NMDA receptor-mediated apoptosis of cerebrocortical neurons. Concomitantly, BA prevented Deltapsi(m) depolarization, promoted recovery of cellular ATP content, and blocked caspase-3 activation. However, in the presence of BA, Cyt c was still released. Because BA prevented NMDA-induced caspase-3 activation and apoptosis, the presence of Cyt c in the neuronal cytoplasm is not sufficient for the induction of caspase activity or apoptosis. In contrast to these findings, BA was ineffective in preventing staurosporine-induced activation of caspases or apoptosis. Additionally, staurosporine-induced, but not NMDA-induced, apoptosis was associated with activation of caspase-8. These results indicate that, in cerebrocortical cultures, excessive NMDA receptor activation precipitates neuronal apoptosis by means of mitochondrial dysfunction, whereas staurosporine utilizes a distinct pathway. (+info)
Mitochondrial amplification of death signals determines thymidine kinase/ganciclovir-triggered activation of apoptosis. (6/100)Previous clinical experience shows that the efficacy of suicide gene transfer in tumor therapy is limited, resulting from inefficient gene transfer or alternatively, from intrinsic resistance of the tumor in vivo. Herpes simplex virus thymidine kinase/ganciclovir (TK/GCV), a paradigmatic suicide gene therapy system, has been described to exert its cytotoxic effect, at least in part, by inducing apoptosis in target cells. Here, we report that mitochondria amplify TK/GCV-induced apoptosis by regulating p53 accumulation and the effector phase of apoptosis. Treatment with TK/GCV led to mitochondrial perturbations including loss of the mitochondrial membrane potential and release of cytochrome c from mitochondria into the cytosol, inducing caspase activation and nuclear fragmentation. Inhibition of TK/GCV-induced mitochondrial perturbations by Bcl-2 overexpression or by the mitochondrion-specific inhibitor bongkrekic acid also strongly inhibited TK/GCV-induced activation of caspases and apoptosis. TK/GCV-induced mitochondrial perturbations depended on caspase activity possibly initiated by death receptor signaling. Perturbation of mitochondrial function mediated accumulation of wild-type p53 protein, since Bcl-2 overexpression, bongkrekic acid, or inhibition of mitochondrial protein synthesis with chloramphenicol strongly reduced TK/GCV-induced accumulation of wild-type p53 protein. These findings suggest that TK/GCV therapy may be less efficient in tumors in which the mitochondrial amplification of TK/GCV-induced apoptosis is blocked, e.g., by Bcl-2 overexpression. Given the low efficacy of currently used gene therapy systems, our data on molecular mechanisms that regulate sensitivity or resistance toward TK/GCV-induced cytotoxicity might have important implications to improve the clinical application of suicide gene therapy. (+info)
BNIP3 and genetic control of necrosis-like cell death through the mitochondrial permeability transition pore. (7/100)Many apoptotic signaling pathways are directed to mitochondria, where they initiate the release of apoptogenic proteins and open the proposed mitochondrial permeability transition (PT) pore that ultimately results in the activation of the caspase proteases responsible for cell disassembly. BNIP3 (formerly NIP3) is a member of the Bcl-2 family that is expressed in mitochondria and induces apoptosis without a functional BH3 domain. We report that endogenous BNIP3 is loosely associated with mitochondrial membrane in normal tissue but fully integrates into the mitochondrial outer membrane with the N terminus in the cytoplasm and the C terminus in the membrane during induction of cell death. Surprisingly, BNIP3-mediated cell death is independent of Apaf-1, caspase activation, cytochrome c release, and nuclear translocation of apoptosis-inducing factor. However, cells transfected with BNIP3 exhibit early plasma membrane permeability, mitochondrial damage, extensive cytoplasmic vacuolation, and mitochondrial autophagy, yielding a morphotype that is typical of necrosis. These changes were accompanied by rapid and profound mitochondrial dysfunction characterized by opening of the mitochondrial PT pore, proton electrochemical gradient (Deltapsim) suppression, and increased reactive oxygen species production. The PT pore inhibitors cyclosporin A and bongkrekic acid blocked mitochondrial dysregulation and cell death. We propose that BNIP3 is a gene that mediates a necrosis-like cell death through PT pore opening and mitochondrial dysfunction. (+info)
Bcl-2 independence of flavopiridol-induced apoptosis. Mitochondrial depolarization in the absence of cytochrome c release. (8/100)The new chemotherapeutic agent, flavopiridol, presently in clinical trials, has been extensively studied yet little is known about its mechanism of action. In this study we show that the induction of apoptosis by flavopiridol is largely independent of Bcl-2. This is indicated by the observation that neither overexpression nor the antisense oligonucleotide-mediated down-regulation of Bcl-2 had any effect on flavopiridol-induced cell killing. Our results suggest that flavopiridol can induce apoptosis through different pathways of caspase activation with caspase 8 playing a pivotal role. In human lung carcinoma cells, which contain high levels of endogenous Bcl-2 and lack procaspase 8, flavopiridol treatment leads to mitochondrial depolarization in the absence of cytochrome c release, followed by the activation of caspase 3 and cell death. These results clearly differ from observations made with other anti-tumor drugs and might explain, at least in part, the unusual anti-tumor properties of flavopiridol. (+info)
Another inhibitor, bongkrekic acid, is believed to stabilize a second conformation, with the pit facing the matrix. In this ... amino acids, keto acids and cofactors across the membrane. Such proteins include: ADP/ATP carrier protein (ADP-ATP translocase ... 4P5W Mitochondrial carriers transport amino acids, keto acids, nucleotides, inorganic ions and co-factors through the ... "Functional and structural role of amino acid residues in the even-numbered transmembrane alpha-helices of the bovine ...
Mitochondrial permeability transition pore
... bongkrekic acid and alisporivir (also known as Debio-025). TRO40303 is a newly synthetitised MPT blocker developed by Trophos ... Other factors that increase the likelihood that the MPTP will be induced include the presence of certain fatty acids, and ...
In contrast, the second family, which includes bongkrekic acid (BA) and isobongkrekic acid (isoBA), binds the translocase from ...
... (also known as bongkrekic acid) is a respiratory toxin more deadly than other mitochondrial poisons cyanide or 2, ... Garcia, R. A.; Hotchkiss, J. H.; Steinkraus, K. H. (1999). "The Effect of Lipids on Bongkrekic (Bongkrek) Acid Toxin Production ... Henderson, P. J. F.; Lardy, H. A. (1970). "Bongkrekic Acid: An Inhibitor of Adenine Nucleotide Translocase of Mitochondria" ( ... "Structure of Bongkrekic Acid". Tetrahedron. 29 (11): 1541-1547. doi:10.1016/S0040-4020(01)83395-0. Bhavbhuti M. Mehta, Afaf ...
List of MeSH codes (D02)
2-aminoadipic acid MeSH D02.241.081.337.052.250 --- dimethyl adipimidate MeSH D02.241.081.337.075 --- bongkrekic acid MeSH ... edetic acid MeSH D02.241.081.038.455 --- egtazic acid MeSH D02.241.081.038.581 --- iodoacetic acid MeSH D02.241.081.038.581.400 ... muramic acids MeSH D02.241.081.844.562 --- neuraminic acids MeSH D02.241.081.844.562.668 --- sialic acids MeSH D02.241.081.844. ... quinic acid MeSH D02.241.511.852 --- shikimic acid MeSH D02.241.511.902 --- sugar acids MeSH D02.241.511.902.107 --- ascorbic ...
Mozambique funeral beer poisoning
... bongkrekic acid and toxoflavin, in both the beer and the corn flour that was used to help brew it, and concluded that these ... Nyazema, N. Z. (June 1985). "Crocodile (Crocodylus niloticus) bile acids and arrow poisons". Central African Journal of ...
We have beforehand claimed that glutamate and the adenine nucleotide translocase inhibitor, carboxyatractyloside, ameliorate...
As in the rabbit, dBSA tended to enhance the CCCP fee, but this was only major for succinate alone (P,.05). Not like the rabbit tubules, basal and oligomycin
Bongkrekic acid (BKA) is a strong inhibitor of adenine nucleotide translocase (ANT), inducing inhibition of adenosine triphosphate synthesis. We designed and synthesized simplified benzene-ring-containing BKA analogs. The key reaction is the one-pot double Sonogashira reaction, which forms the main skeleton. The analogs were efficiently synthesized in 8-10 longest linear sequence steps. This synth ...
AMDs upcoming six-core desktop processor, the Phenom II X6, will introduce a new feature to the Phenom II series, currently known as C-state performance...
Hi solomon levi, I havent had internet for the past few weeks, but I would like to give you an update on my work. Ive consumed a small amount of liquid Dead S
This is the first Hoodia product I have ever bought, and I was skeptical to try it, but it has been working GREAT! I have been taking it for about two weeks, and in the last week I have lost about a pound a day! I have just been trying to lose like 12 pounds for the last year, but I have not been able to do it. I eat healthily and exercise, but I just never feel full, so I guess I eat too much in one sitting. The Hoodia helped me eat less and then not feel like Im starving. I count my calories too, and one day I ate less than 1000 calories and felt fine. Its good stuff, and I am so glad that I found it. If you have will power, (because you can still eat if you want to) this product is awesome. ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~I have found this Hoodia to work well when other brands I tried did not. My trainer at the gym recommended hoodia in general but not a paticular brand. She said that some brands work better than others. This is my ...
Mitochondrial carriers are believed widely to be homodimers both in the inner membrane of the organelle and in detergents. The dimensions and molecular masses of the detergent and protein-detergent micelles were measured for yeast ADP/ATP carriers in a range of different detergents. The radius of the carrier at the midpoint of the membrane, its average radius, its Stokes radius, its molecular mass, and its excluded volume were determined. These parameters are consistent with the known structural model of the bovine ADP/ATP carrier and they demonstrate that the yeast mitochondrial ADP/ATP carriers are monomeric in detergents. Therefore, models of substrate transport have to be considered in which the carrier operates as a monomer rather than as a dimer.. ...
Structures of yeast mitochondrial ADP/ATP carriers support a domain-based alternating-access transport mechanism. | MRC...
The mitochondrial ADP/ATP carrier imports ADP from the cytosol and exports ATP from the mitochondrial matrix. The carrier cycles by an unresolved mechanism between the cytoplasmic state, in which the carrier accepts ADP from the cytoplasm, and the matrix state, in which it accepts ATP from the mitochondrial matrix. Here we present the structures of the yeast ADP/ATP carriers Aac2p and Aac3p in the cytoplasmic state. The carriers have three domains and are closed at the matrix side by three interdomain salt-bridge interactions, one of which is braced by a glutamine residue. Glutamine braces are conserved in mitochondrial carriers and contribute to an energy barrier, preventing the conversion to the matrix state unless substrate binding occurs. At the cytoplasmic side a second salt-bridge network forms during the transport cycle, as demonstrated by functional analysis of mutants with charge-reversed networks. Analyses of the domain structures and properties of the interdomain interfaces indicate ...
Adenine nucleotide translocator synonyms, Adenine nucleotide translocator antonyms - FreeThesaurus.com
Synonyms for Adenine nucleotide translocator in Free Thesaurus. Antonyms for Adenine nucleotide translocator. 1 synonym for adenine: A. What are synonyms for Adenine nucleotide translocator?
Adenine Nucleotide Translocator 1: A subtype of mitochondrial ADP, ATP translocase found primarily in heart muscle (MYOCARDIUM) and skeletal muscle (MUSCLE, SKELETAL).
Rabbit polyclonal Adenine Nucleotide Translocator 2 antibody validated for WB, IP and tested in Human. With 2 independent reviews. Immunogen corresponding to…
Adenine nucleotide translocator 1 | definition of adenine nucleotide translocator 1 by Medical dictionary
Looking for online definition of adenine nucleotide translocator 1 in the Medical Dictionary? adenine nucleotide translocator 1 explanation free. What is adenine nucleotide translocator 1? Meaning of adenine nucleotide translocator 1 medical term. What does adenine nucleotide translocator 1 mean?
Mitochondrial permeability transition pore component cyclophilin D distinguishes nigrostriatal dopaminergic death paradigms in...
Mitochondrial permeability transition pore component cyclophilin D distinguishes nigrostriatal dopaminergic death paradigms in the MPTP mouse model of Parkinsons disease Academic Article ...
Slc25a4 (untagged) - Mouse solute carrier family 25 (mitochondrial carrier, adenine nucleotide translocator), member 4 (cDNA...
Slc25a4 (untagged) - Mouse solute carrier family 25 (mitochondrial carrier, adenine nucleotide translocator), member 4 (cDNA clone, (10ug), 10 µg.
Slc25a13 (untagged) - Mouse solute carrier family 25 (mitochondrial carrier, adenine nucleotide translocator), member 13 ...
Slc25a13 (untagged) - Mouse solute carrier family 25 (mitochondrial carrier, adenine nucleotide translocator), member 13 (Slc25a13), nuclear gene encoding mitochondrial protein, transcript variant 1, (10ug), 10 µg.
Activation of the mitochondrial permeability transition pore (PTP) clearly plays a key role in some of the most wide-spread and therapeutically challenging huma...
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Graham BH et al. (1997) A mouse model for mitochondrial myopathy and cardiomyopathy resulting from a deficiency in the heart/muscle isoform of the adenine nucleotide translocator.. [^] ...
TY - JOUR. T1 - The mitochondrial permeability transition from in vitro artifact to disease target. AU - Bernardi, Paolo. AU - Krauskopf, Alexandra. AU - Basso, Emy. AU - Petronilli, Valeria. AU - Blalchy-Dyson, Elizabeth. AU - Di Lisa, Fabio. AU - Forte, Michael. PY - 2006/5. Y1 - 2006/5. N2 - The mitochondrial permeability transition pore is a high conductance channel whose opening leads to an increase of mitochondrial inner membrane permeability to solutes with molecular masses up to ≈1500 Da. In this review we trace the rise of the permeability transition pore from the status of in vitro artifact to that of effector mechanism of cell death. We then cover recent results based on genetic inactivation of putative permeability transition pore components, and discuss their meaning for our understanding of pore structure. Finally, we discuss evidence indicating that the permeability transition pore plays a role in pathophysiology, with specific emphasis on in vivo models of disease.. AB - The ...
Abstract 3314: Opening of the Mitochondrial Permeability Transition Pore is Not Precluded With Cyclosporine A in vivo During...
Objective: A mechanism of mitochondrial injury during ischemia/reperfusion is Ca2+-induced opening of the mitochondrial permeability transition pore (mPTP). We examined whether cyclosporine A (CsA), an mPTP inhibitor, could benefit resuscitation in a rat model of cardiac arrest. We also assessed whether CsA prevents Ca2+ mediated mPTP opening in isolated mitochondria using a swelling assay.. Methods: VF was induced and left untreated for 10 mins. Resuscitation was attempted by 8 mins of chest compression and defibrillation, observing the rats for 360 mins post-resuscitation (PR). Rats were randomized to receive 10 mg/kg CsA (n=6) or vehicle (n=3) before inducing VF or 10 mg/kg CsA (n=6) or vehicle (n=3) before starting chest compression. CsA treated and vehicle treated subgroups were pooled for the analysis. Four rats not subjected to cardiac arrest served as sham. Mitochondrial NAD+ levels in hearts harvested after the PR interval served as indirect marker of mPTP opening. Mitochondria isolated ...
SLC25A31 antibody (solute carrier family 25 (mitochondrial carrier; adenine nucleotide translocator), member 31) for ELISA, WB. Anti-SLC25A31 pAb (GTX87816) is tested in Human, Mouse samples. 100% Ab-Assurance.
... ,The MitoPT kit is used in conjunction with your existing apoptosis protocols. Grow your cells in culture and induce apoptosis according to your existing procedure (also reserve a non-induced population of cells as a negative control). Once you have induced apoptosis in your cells, add the 1X MitoPT,biological,biology supply,biology supplies,biology product
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Repositorio da Producao Cientifica e Intelectual da Unicamp: Participation of the mitochondrial permeability transition pore in...
In the present study, we investigated the involvement of the mitochondrial permeability transition pore (PTP) in nitric oxide (NO)-induced plant cell death. NO donors such as sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine inhibited growth and caused death in suspension-cultured cells of Citrus sinensis. Cells treated with SNP showed chromatin condensation and fragmentation, characteristic of apoptosis. SNP caused loss of the mitochondrial membrane electrical potential, which was prevented by cyclosporin A (CsA), a specific inhibitor of PTP formation. CsA also prevented the nuclear apoptosis and subsequent Citrus cell death induced by NO. These findings indicate that mitochondrial PTP formation is involved in the signaling pathway by which NO induces apoptosis in cultured Citrus cells. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved ...
Transient Opening of the Mitochondrial Permeability Transition Pore Induces Microdomain Calcium Transients in Astrocyte...
Astrocytes extend highly branched processes that form functionally isolated microdomains, facilitating local homeostasis by redistributing ions, removing neurotransmitters, and releasing factors to influence blood flow and neuronal activity. Microdomains exhibit spontaneous increases in calcium (Ca2+), but the mechanisms and functional significance of this localized signaling are unknown. By developing conditional, membrane-anchored GCaMP3 mice, we found that microdomain activity that occurs in the absence of inositol triphosphate (IP3)-dependent release from endoplasmic reticulum arises through Ca2+ efflux from mitochondria during brief openings of the mitochondrial permeability transition pore. These microdomain Ca2+ transients were facilitated by the production of reactive oxygen species during oxidative phosphorylation and were enhanced by expression of a mutant form of superoxide dismutase 1 (SOD1 G93A) that causes astrocyte dysfunction and neurodegeneration in amyotrophic lateral sclerosis ...
Atractyloside (ATR) is a natural, toxic glycoside and an effective ADP/ATP translocase inhibitor. Atractyloside is synthesized by some plant species in the daisy family e.g. Callilepis laureola, Xanthium strumarium, Iphiona alsoeri, and Pascalia glauca. The poisonous effect of the distaff thistle (and by extension atractyloside) is well documented in history. The plant growing in the Mediterranean region was often used for suicide or murder. Examples of accidental poisoning are documented in Italy and Algeria in 1955 and 1975 respectively, where children have eaten parts of the plant. Although Ed Lefranc[who?] isolated Atractyloside in 1868 from Atractylis gummifera, the structure was identified 100 years later. Atractyloside is a hydrophilic glycoside. A modified glucose is linked to the hydrophobic diterpene atractyligenin by a β1-glycosidic bond. A carboxyl group is positioned at the C4 position in the axial position. The glucose part is esterified with isovaleric acid on the C2 atom, and ...
Cyclophilin D-dependent Mitochondrial Permeability Transition Regulates Some Necrotic but Not Apoptotic Cell Death - PubMed
Mitochondria play an important role in energy production, Ca2+ homeostasis and cell death. In recent years, the role of the mitochondria in apoptotic and necrotic cell death has attracted much attention. In apoptosis and necrosis, the mitochondrial permeability transition (mPT), which leads to disru …
31P NMR and Electron Microscopy on Lipid-Protein Interactions of the Reincorporated ADP/ATP Carrier Protein from Mitochondria |...
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van der Doef TF, de Witte LD, Sutterland AL, Jobse E, Yaqub M, Boellaard R, de Haan L, Eriksson J, Lammertsma AA, Kahn RS, van Berckel BNM, In vivo (R)-[(11)C]PK11195 PET imaging of 18kDa translocator protein in recent onset psychosis. NPJ SCHIZOPHR 2016;2:16031 [PubMed] ...
Bongkrekic acid | CAS 11076-19-0 | SCBT - Santa Cruz Biotechnology
Buy Bongkrekic acid (CAS 11076-19-0), an apoptosis inhibitor through prevention of PARP cleavage, from Santa Cruz. Purity: ≥98 ... Bongkrekic acid (CAS 11076-19-0) Bongkrekic acid , CAS 11076-19-0 is rated 5.0 out of 5 by 1. ... Bongkrekic acid is a mitochondrial permeability transition pore blocker that acts as an inhibitory ligand of the mitochondrial ... PubMed ID 15063741) used bongkrekic acid to inhibit mitochondrial adenine nucleotide translocase 3 (ANT3)-mediated apoptosis in ...https://www.scbt.com/scbt/product/bongkrekic-acid-11076-19-0/
Associated Effluxes of Calcium and Adenine Nucleotides from Mitochondria: Mediation by Thyroxine and other Agents, and...
... and Inhibition by Bongkrekic Acid and Adenosine Diphosphate. MUTHANNA H. AL-SHAIKHALY, HAROLD BAUM ... and Inhibition by Bongkrekic Acid and Adenosine Diphosphate Message Subject (Your Name) has forwarded a page to you from ... and Inhibition by Bongkrekic Acid and Adenosine Diphosphate ... and Inhibition by Bongkrekic Acid and Adenosine Diphosphate ...http://www.biochemsoctrans.org/content/7/1/215
Bongkrek acid - Wikipedia
Bongkrek acid (also known as bongkrekic acid) is a respiratory toxin more deadly than other mitochondrial poisons cyanide or 2, ... Garcia, R. A.; Hotchkiss, J. H.; Steinkraus, K. H. (1999). "The Effect of Lipids on Bongkrekic (Bongkrek) Acid Toxin Production ... Henderson, P. J. F.; Lardy, H. A. (1970). "Bongkrekic Acid: An Inhibitor of Adenine Nucleotide Translocase of Mitochondria" ( ... "Structure of Bongkrekic Acid". Tetrahedron. 29 (11): 1541-1547. doi:10.1016/S0040-4020(01)83395-0. Bhavbhuti M. Mehta, Afaf ...https://en.wikipedia.org/wiki/Bongkrek_acid
The mitochondrial transporter family (SLC25): physiological and pathological implications | SpringerLink
McGivan (1992) Amino acid transport in mitochondria. In: Kilberg MS, Häussinger D (eds) Mammalian amino acid transport. Plenum ... bongkrekic acid. CAC. carnitine/acylcarnitine carrier. CATR. carboxyatractyloside. CoA. coenzyme A. CIC. citrate carrier ... Aquila H, Misra D, Eulitz M, Klingenberg M (1982) Complete amino acid sequence of the ADP/ATP carrier from beef heart ... since their polypeptide chains consist of three tandemly related sequences of about 100 amino acids, and the repeats of the ...https://link.springer.com/article/10.1007%2Fs00424-003-1099-7
Distinct Effects of Saturated and Monounsaturated Fatty Acids on β-Cell Turnover and Function | Diabetes
Effect of bongkrekic acid. J Cell Biol 56: 65-73, 1973. OpenUrlAbstract/FREE Full Text ... alone or with fatty acids (0.5 mmol/l palmitic acid, 0.5 mmol/l palmitoleic acid, or a mixture of 0.25 mmol/l or 0.5 mmol/l ... C for palmitic acid) compared with unsaturated fatty acids (0.5°C for palmitoleic acid). Consequently, triacylglycerols ... 0.05 for the difference between palmitic acid and palmitoleic acid or fatty acid mixture. ...http://diabetes.diabetesjournals.org/content/50/1/69.long
Calcium, mitochondria and reperfusion injury: a pore way to die | Biochemical Society Transactions | Portland Press
... bongkrekic acid) that inhibits pore opening . CAT and BKA are known to induce two quite distinct conformation of the ANT. ... The MPTP is potently inhibited by low pH, and thus only as the pH returns to normal through the loss of lactic acid and the ... Fatty acid oxidation is known to be detrimental to heart function during reperfusion . ... adenine nucleotide depletion and the build-up of lactic acid, with a consequent drop in intracellular pH. In an attempt to ...https://portlandpress.com/biochemsoctrans/article-abstract/34/2/232/63714/Calcium-mitochondria-and-reperfusion-injury-a-pore?redirectedFrom=fulltext
... bongkrekic acid; BAPTA/AM, 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid; CsA, cyclosporin A; CsH, cyclosporin H; ...http://cancerres.aacrjournals.org/content/61/10/3894
Mitochondrial carrier - Wikipedia
Another inhibitor, bongkrekic acid, is believed to stabilize a second conformation, with the pit facing the matrix. In this ... amino acids, keto acids and cofactors across the membrane. Such proteins include: ADP/ATP carrier protein (ADP-ATP translocase ... 4P5W Mitochondrial carriers transport amino acids, keto acids, nucleotides, inorganic ions and co-factors through the ... "Functional and structural role of amino acid residues in the even-numbered transmembrane alpha-helices of the bovine ...https://en.wikipedia.org/wiki/Mitochondrial_carrier
Jasmonates: Novel Anticancer Agents Acting Directly and Selectively on Human Cancer Cell Mitochondria | Cancer Research
... bongkrekic acid + methyl jasmonate (BA + MJ)-treated (•) and bongkrekic acid + cyclosporine A + methyl jasmonate (BA + CSA + MJ ... Cyclosporine A (CSA) at 10 μmol/L and/or bongkrekic acid (BA) at 50 μmol/L were added 15 minutes before the addition of methyl ... Cyclosporine A and bongkrekic acid prevented the effect of methyl jasmonate ( Fig. 3B). In contrast, methyl jasmonate and ... Methyl jasmonate at 1 mmol/L, with or without cyclosporine A (0.25 μmol/L) and/or bongkrekic acid (50 μmol/L) was added for 24 ...http://cancerres.aacrjournals.org/content/65/5/1984.full
17-Allylamino-17-demethoxygeldanamycin enhances the lethality of deoxycholic acid in primary rodent hepatocytes and established...
For studies using cyclosporin A (CsA; 1 μmol/L) or bongkrekic acid (BA; 50 μmol/L), cells were pretreated before 17AAG/DCA ... and the secondary bile acid deoxycholic acid (DCA) in hepatocytes and fibroblasts. DCA and 17AAG interacted in a greater than ... Bile acid regulation of C/EBPβ, CREB, and c-Jun function, via the extracellular signal-regulated kinase and c-Jun NH2-terminal ... Bile acids enhance the activity of the insulin receptor and glycogen synthase in primary rodent hepatocytes. Hepatology 2004;39 ...https://mct.aacrjournals.org/content/6/2/618?ijkey=bf5a7bbaf7be7ec4a37c57c5755c5b0da5c41b75&keytype2=tf_ipsecsha
Palmitoyl-carnitine increases RyR2 oxidation and sarcoplasmic reticulum Ca2+ leak in cardiomyocytes: Role of adenine nucleotide...
Finally, both bongkrekic acid and NAC significantly reduced spontaneous Ca(2+) wave occurrences under PC. Altogether, these ... Inhibition of ANT by bongkrekic acid (20 μM) prevented PC-induced mitochondrial ROS production. In addition, PC increased type ... Long chain fatty acids bind to carnitine and form long chain acyl carnitine (LCAC), to enter into the mitochondria. They are ...https://www.ncbi.nlm.nih.gov/pubmed/25619687
Science Clips - Volume 9, Issue 48, December 5, 2017
Toxic levels of bongkrekic acid (BA) were detected in the suspect pombe but not in the control pombe. Burkholderia gladioli ... Description of a mass poisoning in a rural district in Mozambique: The first documented bongkrekic acid poisoning in Africa ... and nucleic acid-based carbapenemase detection tests that identify carbapenemase activity directly or their associated ...https://www.cdc.gov/library/sciclips/issues/v9issue48.html
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Sulfate and phosphate are also transported using an antiport mechanism (Todisco et al. 2014). Inhibited by bongkrekic acid. ... The mitochondrial basic amino acid transporter, in mBAC1 (transports the basic L-amino acids arginine, lysine, ornithine, and ... Basic amino acid carrier2, BAC2 of 296 aas and 6 TMSs. This hyperosmotic stress-inducible porter transports proline in addition ... The main physiological role of SLC25A29 is to import basic amino acids into mitochondria for mitochondrial protein synthesis ...http://tcdb.org/search/result.php?tc=2.A.29.7
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Sulfate and phosphate are also transported using an antiport mechanism (Todisco et al. 2014). Inhibited by bongkrekic acid. ... The mitochondrial basic amino acid transporter, in mBAC1 (transports the basic L-amino acids arginine, lysine, ornithine, and ... Basic amino acid carrier2, BAC2 of 296 aas and 6 TMSs. This hyperosmotic stress-inducible porter transports proline in addition ... The main physiological role of SLC25A29 is to import basic amino acids into mitochondria for mitochondrial protein synthesis ...http://tcdb.org/search/result.php?tc=2.A.29.23
KAKEN - Research Projects | Elucidaton of molecular mechanism of remodeling for cardiolipin (KAKENHI-PROJECT-26450139)
Journal Article] Bongkrekic Acid Analogue, Lacking One of the Carboxylic Groups of its Parent Compound, Shows Moderate but pH- ... Journal Article] Efficient Total Synthesis of Bongkrekic Acid and Apoptosis Inhibitory Activity of its Analogues2015. *. Author ...https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-26450139/
Inhibitors | Cellular Process | Inhibitors Apoptosis | Inhibitors definition - AG Scientific
Bongkrekic Acid B-1053 Starting at $229.50 Options. 100 ug $229.50. Add to Cart ...https://agscientific.com/cell-biology/inhibitors.html?p=2
Mitochondria in energy-limited states: mechanisms that blunt the signaling of cell death | Journal of Experimental Biology
ADP and bongkrekic acid) (Brustovetsky et al., 2002). However, the occurrence of an in vivo MPTP in N. crassa mitochondria was ... Bcl-2 protects against apoptosis induced by antimycin A and bongkrekic acid without restoring cellular ATP levels. Biochim. ...http://jeb.biologists.org/content/211/12/1829
Liu S[au] - PubMed - NCBI
Bongkrekic acid poisoning: Severe liver function damage combined with multiple organ failure caused by eating spoiled food. ... Fusaric acid instigates the invasion of banana by Fusarium oxysporum f. sp. cubense TR4. ...https://www.ncbi.nlm.nih.gov/pubmed?cmd=search&term=Liu+S%5Bau%5D&dispmax=50
Abstract: A fluorescence-based technique for screening compounds that protect against damage to brain mitochondria
These events were blocked by cyclosporin A (CsA) or Bongkrekic acid (BKA), inhibitors of the mitochondrial permeability ... Antioxidants Energy Supplements Essential Fatty Acids Multi Vitamins Probiotics Vitamins See More ». Amino Acids Minerals ...http://www.prohealth.com/library/showarticle.cfm?libid=10742
Inhibition of the mitochondrial ATP/ADP translocase by bongkrekic acid, which prevents ATP export from the mitochondrion, also ... Increases in cytosolic LC-CoA in the β-cell can result from glucose metabolism and from free fatty acids (FFAs) delivered by ... However, truncation of the last 26-36 amino acids from Kir6.2 (Kir6.2ΔC) allows this subunit to reach the surface membrane in ...http://diabetes.diabetesjournals.org/content/53/suppl_3/S113
Frontiers | The Mitochondrial Permeability Transition Pore and Cancer: Molecular Mechanisms Involved in Cell Death | Oncology
The MPT inhibitor bongkrekic acid (14) inhibits cell death, while the MPT inducer atractyloside (9) renders the cell more ... Nucleic Acids Res (2003) 31:1364-73. doi:10.1093/nar/gkg205. Pubmed Abstract , Pubmed Full Text , CrossRef Full Text , Google ... A unified nomenclature and amino acid numbering for human PTEN. Sci Signal (2014) 7:e15. doi:10.1126/scisignal.2005560 ... Although the effect of retinoic acid on mPTPs was not addressed, this study supports the possibility that cancer cells have ...https://www.frontiersin.org/articles/10.3389/fonc.2014.00302/full
Stimulation of mitochondrial calcium ion efflux by thiol-specific reagents and by thyroxine. The relationship to adenosine...
Both efflux rates were kept at a low value by bongkrekic acid added before the stimulating agent. It is concluded that Ca2+ ...http://www.biochemj.org/content/182/2/455
β-Phenylethyl isothiocyanate mediated apoptosis; Contribution of Bax and the mitochondrial death pathway | [email protected]
Bongkrekic acid. CsA. cyclosporine A. glutathione. GSH. mBCl. mitochondrial membrane potential. mitochondrial permeability ... Accordingly, using pharmacological inhibitors of MPT namely cyclosporine A, trifluoperazine and Bongkrekic acid we were unable ...http://scholarbank.nus.edu.sg/handle/10635/32001
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Toxic levels of bongkrekic acid (BA) were detected in the suspect pombe but not in the control pombe. Burkholderia gladioli ... Description of a mass poisoning in a rural district in Mozambique: The first documented bongkrekic acid poisoning in Africa ...https://stacks.cdc.gov/view/cdc/53615
- Bongkrekic acid is a mitochondrial permeability transition pore blocker that acts as an inhibitory ligand of the mitochondrial adenine nucleotide translocator. (scbt.com)
- PubMed ID 15063741) used bongkrekic acid to inhibit mitochondrial adenine nucleotide translocase 3 (ANT3)-mediated apoptosis in cultured cells. (scbt.com)
- Here we examine the effect of saturated and unsaturated fatty acids at different glucose concentrations on β-cell proliferation and apoptosis. (diabetesjournals.org)
- The cell-permeable ceramide analog C 2 -ceramide mimicked both the palmitic acid-induced β-cell apoptosis and decrease in proliferation. (diabetesjournals.org)
- Taken together, these results suggest that the lipotoxic effect of the saturated palmitic acid involves an increased apoptosis rate coupled with reduced proliferation capacity of β-cells and impaired insulin secretion. (diabetesjournals.org)
- In contrast, the monounsaturated palmitoleic acid does not affect β-cell apoptosis, yet it promotes β-cell proliferation at low glucose concentrations, counteracting the negative effects of palmitic acid as well as improving β-cell function. (diabetesjournals.org)
- In an adipogenic model of diabetes, the Zucker diabetic fatty rat, fatty acid-induced β-cell apoptosis was observed ( 5 ). (diabetesjournals.org)
- SNAP-induced apoptosis was suppressed by inhibitor of mPT bongkrekic acid (BA), inhibitor of JNK SP600125 and superoxide dismutase-mimetic AEOL 10150. (uta.fi)
- Inhibition of ANT by bongkrekic acid (20 μM) prevented PC-induced mitochondrial ROS production. (nih.gov)
- Effects of genetic and pharmacological inhibition of the MPTP were examined in isolated murine and human pancreatic acinar cells, and in hyperstimulation, bile acid, alcoholic and choline-deficient, ethionine-supplemented acute pancreatitis. (bmj.com)
- 3) to result from a preferen- tial inhibition by the analog for non-en- ergy-linked membrane-bound ATPase. (pdfslide.net)
- Increasing concentrations of glucose promoted β-cell proliferation that was dramatically reduced by palmitic acid. (diabetesjournals.org)
- Palmitoleic acid enhanced the proliferation activity in medium containing 5.5 mmol/l glucose but had no additional effect at higher glucose concentrations (11.1 and 33.3 mmol/l). (diabetesjournals.org)
- 2. Cyclosporin (1 microM) had no significant effect on the swelling induced by butyrate, bongkrekic acid or Ca2+ at concentrations of less than 0.3 microM. (portlandpress.com)
- These data together with observations that palmitate does not increase H+ conductance in bilayer phospholipid membranes and in cytochrome oxidase-asolectin proteoliposomes indicate that the ATP/ADP-antiporter is somehow involved in the uncoupling by low concentrations of fatty acids (or DNP), whereas that by FCCP and gramicidin D is due to their effect on the phospholipid bilayer. (msu.ru)
- Bongkrek acid (also known as bongkrekic acid) is a respiratory toxin more deadly than other mitochondrial poisons cyanide or 2,4-dinitrophenol. (wikipedia.org)
- There was some dispute regarding the actual structure of bongkrek acid, but this was resolved in 1973, which explains different structures appearing in the literature prior to this date. (wikipedia.org)
- Exposure of islets to saturated fatty acid (0.5 mmol/l palmitic acid) in medium containing 5.5, 11.1, or 33.3 mmol/l glucose for 4 days resulted in a five- to ninefold increase of β-cell DNA fragmentation. (diabetesjournals.org)
- Apart from hyperglycemia, plasma long-chain free fatty acid levels are often increased in states of insulin resistance, further impairing β-cell-secretory function ( 8 , 9 ). (diabetesjournals.org)
- Carboxyatractylate inhibits the uncoupling effect of free fatty-acids / A. ANDREYEV, T. BONDAREVA, V. DEDUKHOVA et al. (msu.ru)
- Plant derived omega-3-fatty acids protect mitochondrial function in the brain. (labome.org)
- acid (yielding fatty acyl-CoA). (yumpu.com)
- Herein, to better understand how the normal tissue toxicity of geldanamycins could be ameliorated to improve the therapeutic index of these agents, we examined the interactions of 17-allylamino-17-demethoxygeldanamycin (17AAG) and the secondary bile acid deoxycholic acid (DCA) in hepatocytes and fibroblasts. (aacrjournals.org)
- All MCs of known function belong to the same protein family, since their polypeptide chains consist of three tandemly related sequences of about 100 amino acids, and the repeats of the different carriers are homologous. (springer.com)
- In protein science , an Imino Acid (Secondary Amino Acid) is a molecule, related to amino acids (differing in the bonding to the nitrogen), that contains both an imino (>C=NH) and a carboxyl (-C(=O)-OH) functional group, which occurs as either an acyclic acid or a cyclic imino acid . (wellnessadvocate.com)