Relevant bibliographies by topics / Metabolism; Cytosol

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  1. Journal articles
  2. Dissertations / Theses
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  5. Conference papers

Academic literature on the topic 'Metabolism; Cytosol'

Author: Grafiati
Published: 4 June 2021
Last updated: 3 February 2022

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Journal articles on the topic "Metabolism; Cytosol"

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Mikšanová, Markéta, Petr Novák, Eva Frei, and Marie Stiborová. "Metabolism of Carcinogenic 2-Nitroanisole in Rat, Rabbit, Porcine and Human Hepatic Cytosol." Collection of Czechoslovak Chemical Communications 69, no. 3 (2004): 589–602. http://dx.doi.org/10.1135/cccc20040589.

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We investigated the ability of hepatic cytosolic samples from human, rat, rabbit and pig to metabolize an important industrial pollutant and a potent carcinogen for rodents, 2-nitroanisole (1-methoxy-2-nitrobenzene). A comparison between experimental animals and the human enzymatic system is essential for the extrapolation of animal carcinogenicity data to humans to assess a health risk to humans. Two major metabolites produced from 2-nitroanisole by cytosols of all species were N-(2-methoxyphenyl)hydroxylamine and 2-methoxyaniline. An additional minor product of 2-nitroanisole metabolism has not yet been characterized. Both the identified metabolites are generated from 2-nitroanisole by reduction of the nitro group. To define the role of cytosolic reductases in the reduction of 2-nitroanisole, we investigated the modulation of 2-nitroanisole reduction by cofactors of the cytosolic reductases, DT-diaphorase and xanthine oxidase. The role of the human enzymes in 2-nitroanisole reduction was also investigated by correlating the xanthine oxidase-linked catalytic activities in each human cytosolic sample with the concentration of the 2-nitroanisole reduction product, 2-methoxyaniline, formed by the action of the same cytosol. On the basis of these analyses, most of hepatic cytosolic reduction of 2-nitroanisole was attributed to xanthine oxidase, but participation of DT-diaphorase in the reduction of this carcinogen in hepatic cytosols of rabbit and pigs cannot be excluded. Using the purified xanthine oxidase, its participation in 2-nitroanisole reduction was confirmed. The data clearly demonstrate the predominant role of xanthine oxidase in 2-nitroanisole reduction in human and rat hepatic cytosols and suggest a carcinogenic potency of this rodent carcinogen for humans.
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Cruz, Rogério Santos de Oliveira, Rafael Alves de Aguiar, Tiago Turnes, Rafael Penteado Dos Santos, Mariana Fernandes Mendes de Oliveira, and Fabrizio Caputo. "Intracellular Shuttle: The Lactate Aerobic Metabolism." Scientific World Journal 2012 (2012): 1–8. http://dx.doi.org/10.1100/2012/420984.

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Lactate is a highly dynamic metabolite that can be used as a fuel by several cells of the human body, particularly during physical exercise. Traditionally, it has been believed that the first step of lactate oxidation occurs in cytosol; however, this idea was recently challenged. A new hypothesis has been presented based on the fact that lactate-to-pyruvate conversion cannot occur in cytosol, because the LDH enzyme characteristics and cytosolic environment do not allow the reaction in this way. Instead, the Intracellular Lactate Shuttle hypothesis states that lactate first enters in mitochondria and only then is metabolized. In several tissues of the human body this idea is well accepted but is quite resistant in skeletal muscle. In this paper, we will present not only the studies which are protagonists in this discussion, but the potential mechanism by which this oxidation occurs and also a link between lactate and mitochondrial proliferation. This new perspective brings some implications and comes to change our understanding of the interaction between the energy systems, because the product of one serves as a substrate for the other.
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Greger, Janusz, and Fabianowska-Majewska Krystyna. "Different Effect Of Dgtp On 2'-Deoxyadenosine Metabolism In Mitochondria And Cytosol." Zeitschrift für Naturforschung C 47, no. 11-12 (December 1, 1992): 893–97. http://dx.doi.org/10.1515/znc-1992-11-1217.

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Two enzymes participating in 2′-deoxyadenosine (dAdo) metabolism: dAdo kinase (dAdoK EC 2.7.1.76) and adenosine deaminase (ADA, EC 3.5.4.4) were partially purified from rat liver mitochondria and cytosol and influence of nucleosides and nucleotides on the activity of these enzymes were investigated. Mitochondrial and cytosol dAdoK are separate proteins, while ADA from both subcellular fractions possesses similar physical properties. dGTP, a com petitive inhibitor of mitochondrial dAdoK, inhibits cytosol ADA in a mixed way but activates mitochondrial ADA and cytosol dAdoK. A possible effect of dGTP on dAdo metabolism in mitochondria and cytosol is discussed
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Herington, A. C., J. Stevenson, L. Coulson, and S. Ymer. "Characterization of a soluble prolactin-binding activity in rat liver cytosol." Journal of Endocrinology 109, no. 1 (April 1986): 61–66. http://dx.doi.org/10.1677/joe.0.1090061.

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ABSTRACT Soluble binding activity for lactogenic hormones has been detected in high-speed cytosolic preparations from the livers of 21-day-old male and female rats. No lactogenic hormone binding was detected in cytosols from rat heart, kidney, skeletal muscle or adipose tissue. Liver cytosol binding of 125I-labelled human growth hormone or ovine prolactin was dependent on time, temperature, and protein and calcium concentrations. Binding was specific for lactogenic hormones and not somatotrophic hormones. Scatchard analysis revealed linear plots with an affinity of 2·9–4·6 litres/ nmol. By gel filtration the molecular weight of the lactogen-binding activity was > 450 000. The cytosolic binding activity may be an internalized form of the membrane-bound lactogen receptor, which has similar binding characteristics, or alternatively it may be a distinct binding species, with a defined role in mediating intracellular effects of prolactin in the liver. J. Endocr. (1986) 109, 61–66
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Zhou, Lufang, Jennifer E. Salem, Gerald M. Saidel, William C. Stanley, and Marco E. Cabrera. "Mechanistic model of cardiac energy metabolism predicts localization of glycolysis to cytosolic subdomain during ischemia." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 5 (May 2005): H2400—H2411. http://dx.doi.org/10.1152/ajpheart.01030.2004.

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A new multidomain mathematical model of cardiac cellular metabolism was developed to simulate metabolic responses to reduced myocardial blood flow. The model is based on mass balances and reaction kinetics that describe transport and metabolic processes of 31 key chemical species in cardiac tissue. The model has three distinct domains (blood, cytosol, and mitochondria) with interdomain transport of chemical species. In addition to distinguishing between cytosol and mitochondria, the model includes a subdomain in the cytosol to account for glycolytic metabolic channeling. Myocardial ischemia was induced by a 60% reduction in coronary blood flow, and model simulations were compared with experimental data from anesthetized pigs. Simulations with a previous model without compartmentation showed a slow activation of glycogen breakdown and delayed lactate production compared with experimental results. The addition of a subdomain for glycolysis resulted in simulations showing faster rates of glycogen breakdown and lactate production that closely matched in vivo experimental data. The dynamics of redox (NADH/NAD+) and phosphorylation (ADP/ATP) states were also simulated. These controllers are coupled to energy transfer reactions and play key regulatory roles in the cytosol and mitochondria. Simulations showed a similar dynamic response of the mitochondrial redox state and the rate of pyruvate oxidation during ischemia. In contrast, the cytosolic redox state displayed a time response similar to that of lactate production. In conclusion, this novel mechanistic model effectively predicted the rapid activation of glycogen breakdown and lactate production at the onset of ischemia and supports the concept of localization of glycolysis to a subdomain of the cytosol.
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Barlow, John W., Andrea J. Curtis, Lorna E. Raggatt, Nicole M. Loidl, Duncan J. Topliss, and Jan R. Stockigt. "Drug competition for intracellular triiodothyronine-binding sites." European Journal of Endocrinology 130, no. 4 (April 1994): 417–21. http://dx.doi.org/10.1530/eje.0.1300417.

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Barlow JW, Curtis AJ, Raggatt LE, Loidl NM, Topliss DJ. Stockigt JR. Drug competition for intracellular triiodothyronine-binding sites. Eur J Endocrinol 1944;130:417–21. ISSN 0804–4643 A variety of substances, including frusemide, non-esterified fatty acids (NEFAs) and non-steroidal antiinflammatory drugs (NSAIDs), can compete for triiodothyronine (T3)-binding sites in serum and at the cell surface. We examined the competitive potency of these agents at intracellular T3-binding sites in order to assess their potential to act as T3 antagonists. Competition for [125I]T3 binding was determined using hydroxyapatite separation in cytosols and nuclear extracts prepared from livers of Macaca fascicularis. The T3 affinities were 15.8 ± 1.2 nmol/l in cytosol and 0.23 ± 0.02 nmol/l in nuclear extract. Does–response curves were analysed by a four-parameter sigmoid curve-fitting program to determine competitor potency. The nineteen agents tested included various NSAIDs, NEFAs, non-bile acid cholephils (NBACs), frusemide, amiodarone and the flavonoid EMD 21388. In nuclear extract the most active competitors were linoleic acid (8.5 μmol/l) and linolenic acid (7.8 μmol/l), Potencies of NSAIDs varied between 66 μmol/l (meclofenamic acid) and 525 μmol/l (diclofenac). In cytosol, NEFAs were less potent but NSAIDs were stronger competitors than in nuclear extract. Half-inhibitory potencies in cytosol were between 13.2 μmol/l (meclofenamic acid) and 63.1 μmol/l (flufenamic acid). The NBAC bromosulphthalein was one of the most potent inhibitors in both cytosol and nuclear extract. When expressed relative to T3, diclofenac was a more effective competitor in cytosol than it was in nuclear extract. Amiodarone and EMD 21388 were without effect both in cytosol and nuclear extract. Frusemide (759 μmol/l) was weakly active in cytosol only. The action of T3 was assessed by measuring secretion of sex hormone-binding globulin (SHBG) in Hep-G2 cells. After 3 days with total T3 (0.1 μmol/l), SHBG was 155 ± 15% of the control. Amiodarone (100 μmol/l) and meclofenamic acid (100 μmol/l) were cytotoxic. Bromosulphthalein (10 μmol/l), one of the most potent competitors at both the cytoplasmic and the nuclear level, did not influence the T3-induced rise in SHBG secretion. None of the drugs tested affected the magnitude of maximal induction of SHBG by T3. Substances that compete for serum and cell surface T3-binding sites are also weak competitors for intracellular T3-binding proteins, although the heirarchy of potency differs. Frusemide and diclofenac, with a greater relative potency for cytosolic binding than nuclear binding, may have potential use in investigating the function of cytosolic T3-binding. Amiodarone shows no binding activity and is not a hormone antagonist in primate hepatic tissue. John W Barlow, Ewen Downie Metabolic Unit, Alfred Hospital, Commercial Road, Melbourne, Victoria 3181, Australia
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McMorris, Trevor C., Anissa N. Elayadi, Jian Yu, and Michael J. Kelner. "Metabolism of antitumor acylfulvene by rat liver cytosol." Biochemical Pharmacology 57, no. 1 (January 1999): 83–88. http://dx.doi.org/10.1016/s0006-2952(98)00273-1.

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Evans, M. A., R. Bhat, C. Papazafiratou, and D. Vidyasagar. "Effect of Hepatic Cytosol on Postnatal Drug Metabolism." Developmental Pharmacology and Therapeutics 10, no. 3 (1987): 199–211. http://dx.doi.org/10.1159/000457745.

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Penning, Trevor M. "Indomethacin and glucocorticoid metabolism in rat liver cytosol." Biochemical Pharmacology 35, no. 23 (December 1986): 4203–9. http://dx.doi.org/10.1016/0006-2952(86)90696-9.

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Myers, Steven R., Jerry W. Blake, and James W. Flesher. "Metabolism of 3-methylcholanthrene in rat liver cytosol." Chemico-Biological Interactions 71, no. 4 (1989): 393–401. http://dx.doi.org/10.1016/0009-2797(89)90113-0.

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Dissertations / Theses on the topic "Metabolism; Cytosol"

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Marks, Alison J. "The role of cytosolic 6-phosphogluconate dehydrogenase in maize primary roots." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365684.

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Goudard, Françoise. "Contribution a l'etude du metabolisme des radionucleides **(252)cf, **(241)am et **(95m)tc." Nantes, 1987. http://www.theses.fr/1987NANT2019.

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Chave, Karen Judy. "Analysis of variant cytosolic serine hydroxymethyltransferases." Thesis, University of Surrey, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336746.

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Sienkiewicz-Porzucek, Agata. "Evaluation of the role of mitochondrial citrate synthase, mitochondrial and cytosolic isoforms of isocitrate dehydrogenase in tomato leaf metabolism." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2010. http://dx.doi.org/10.18452/16074.

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Der Citratzyklus (TCA) ist einer der bedeutendsten Stoffwechselwege für alle lebenden Organismen. Trotz der zentralen Rolle dieses Prozesses im Pflanzenmetabolismus ist er nur relativ wenig untersucht worden. In dieser Arbeit berichte ich über die Produktion und die funktionale Analyse von Tomatenpflanzen (Solanum lycopersicum), die unabhängig eine leicht eingeschränkte Aktivität der mitochondrialen Citrat-Synthase (CS) und zweier Isocitrat-dehydrogenasen (mitochondriale NAD-IDH und cytosolische NADP-ICDH) zeigen. Die transgene Pflanzen wiesen mehrheitlich keine erkennbare Veränderung eines Wachstumphänotyps auf. Obwohl die photosyntetische Leistung keine Änderungen gezeigt hatte, war die mitochondriale Respiration gestiegen, begleitet von einem reduzierten Kohlenstoff-fluss durch den Citratzyklus. Darüber hinaus waren die CS Pflanzen charakterisiert durch wesentliche Änderungen im Blattmetabolismus, einschließlich eines eingeschränkten Niveaus des photosynthetischen Pigments und Zwischenprodukten des Citratzyklus zusammen mit einer Akkumulation von Nitraten, verschiedenen Aminosäuren und Stärken. Zusammengefasst deuten diese Ergebnisse auf eine Einschränkung der Nitrat-Aufnahme hin. Das mit Hilfe von TOM1 Mikroarrays und quantitativer RT-PCR durchgeführte Transcript-profiling hat gezeigt, dass die fehlende Aktivität der mitochondrialen CS teilweise von einer gestiegenen, peroxisomalen CS Isoform ausgeglichen wird. Die metabolische Verschiebung ergab eine Verstärkung der photorespiratorischen Leistung, die vermutlich eine ausgleichende Rolle in der Produktion organischer Säuren und der Wiederherstellung der Redox-Balance spielt. Interessantenweise war die metabolische Antwort von Blättern auf Stickstoffmangel in NADP-ICDH Pflanzen dramatischer als in NAD-IDH Pflanzen, was darauf hindeutet, dass die cytosolische Isoform der Hauptlieferant von 2-Oxoglutarat im Tomatenmetabolismus sein könnte.
Although the TCA cycle is a respiratory metabolic pathway of central importance for all living organisms, relatively few molecular physiological studies of plants were performed to date. Here, I report the generation and functional analysis of tomato plants (Solanum lycopersicum) independently displaying mildly limited activity of mitochondrial citrate synthase (CS) and two isocitrate dehydrogenases, namely mitochondrial NAD-IDH and cytosolic NADP-ICDH. The transgenic plants revealed minor phenotypic alterations. Although the leaf photosynthetic performance was largely unaltered, the changes in mitochondrial respiration and carbon flux through the TCA cycle were observed. Moreover, the plants were characterized by significant modifications in the leaf metabolic content and in maximal catalytic activities of several enzymes involved in primary C and N metabolism. These results hint towards limitations in nitrate assimilation pathway. The transcript profiling performed by utilizing TOM1 microarrays and quantitative RT-PCR approach revealed that the deficiency in mitochondrial CS activity was partially compensated by up-regulation of peroxisomal CS isoform. The limitations in the activities of isocitrate dehydrogenases resulted in up-regulation of the photorespiratory pathway, which presumably played a compensatory role in supporting organic acid production and re-establishing redox balance in the transgenic leaves. Interestingly, the leaf metabolic response towards nitrogen starvation conditions was far more dramatic in NADP-ICDH transgenic plants than NAD-IDH plants, hinting that the cytosolic isoform may be the major 2-oxoglutarate supplier in tomato metabolism.
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Dekhne, Aamod Sanjeev. "Therapeutic Dual-targeting of Cytosolic and Mitochondrial One-carbon Metabolism." Thesis, Wayne State University, 2021. http://pqdtopen.proquest.com/#viewpdf?dispub=13812930.

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One-carbon metabolism (1CM) is compartmentalized in the mitochondria and cytosol and generates a host of metabolites critical to tumor propagation. Although drug-targeting of cytosolic 1CM remains a clinically-relevant mainstay, development of clinically-useful agents targeting mitochondrial 1CM remains elusive. Of particular pharmacological interest is the mitochondrial 1CM enzyme, serine hydroxymethyltransferase2 (SHMT2). SHMT2 expression correlates with the oncogenic phenotype in lung, colon, breast, glioma, and liver cancer and, overall, is the fifth-most differentially expressed metabolic enzyme in cancer cell versus normal tissue. Despite the unequivocal oncogenic importance and therapeutic potential of SHMT2, there are no clinically relevant (i.e. active in vivo) inhibitors of this enzyme. In this dissertation work, we sought to design, synthesize, and characterize pharmacodynamics of our 5-substituted pyrrolo[3,2-d]pyrimidine antifolates synergistically dual-targeting mitochondrial SHMT2 and cytosolic 1CM, the latter specifically at the purine nucleotide biosynthesis enzymes glycinamide ribonucleotide formyltransferase (GARFTase) and/or 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase (AICARFTase). By depleting SHMT2-derived formate, these compounds potentiated their own inhibition of the downstream formate-dependent GARFTase and AICARFTase. We generated these compounds (AGF291, AGF320, and AGF347) by melding structures of SHMT2 cofactor 5,10-methylene tetrahydrofolate with our previously reported purine inhibitors and confirmed enzyme targets with in vitro targeted metabolomics in H460 (large cell lung carcinoma), HCT-116 (colorectal carcinoma), and MIA PaCa-2 (pancreatic ductal adenocarcinoma) human tumor cell lines as well as in vitro cell-free assays. Transport assays revealed significant uptake by both the proton-coupled folate transporter (narrow physiological niche, but commonly expressed in many solid tumors) and the reduced folate carrier (major tissue folate transporter). Subcellular fractionation of MIA PaCa-2 and GlyB Chinese hamster ovary cells revealed AGF347 to be heavily (>98%) polyglutamylated in both cytosol and mitochondria with mitochondrial uptake partially mediated by the mitochondrial folate transporter. Intracellular glycine depletion secondary to SHMT2 inhibition by all compounds also depleted cellular ROS scavenging capacity as reflected in decreased GSH/GSSG ratio. In vivo, AGF347 demonstrated potent antitumor efficacy against MIA PaCa-2 xenografts in SCID mice with tumor growth delay (T-C) of 61 days and one out of five treated mice tumor-free 120+ days after treatment. In vivo metabolomics on these xenografts confirmed inhibition of purine biosynthesis. Collectively, the work in this dissertation establishes the exceptional therapeutic potential of dual-targeting mitochondrial and cytosolic 1CM.
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Carvalho, FabrÃcio EulÃlio Leite. "Overexpression protein related activities photochemical fotorespiratÃria induced and whisper of contributing to a cytosolic apx submitted to high light." Universidade Federal do CearÃ, 2013. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=11515.

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CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior
In tropical regions, where there is a high incidence of light, electrons can accumulate in the transport chain (PET) producing large quantities of H 2 O 2 and other ROS, which might generate photodamage and photoinhibition. To survive to these challenges, plants have developed several mechanisms to mitigate the excess energy in photosystems, besides having an efficient machinery for removal of excess H 2 O 2 , which includes cytosolic APX (cAPX). However, double - silenced rice plants for cAPX (OsAPX1/2) do not show large differences in morpho - phenotype when compared to non - transformed (NT), although OsAPX1/2 presents induction of expression on several proteins re lated to photosynthesis. The physiological implications of this induction, as well as its consequences for OsAPX1/2 resistance against stresses of high light (HL), are still poorly known. Aiming to clarify the role of cAPx in pho tosynthesis, OsAPX1/2 plant s were produced, subjected to 24 hours of HL (2 , 000 μ mol m - 2 s - 1 ) and studied for the expression and activity of proteins related to photosynthesis , ph otorespira tion and redox homeostasis . The amount of several PET proteins (Lhcb1, PsbO, Psb P, PsbQ, PSAC, P C, FNR and FDX) and Chl and Pheo were increased in OsAPX1/2 in normal growth conditions, however without causing changes in the in vivo photochemistry activity parameters (Fv /Fm and ΔFm/Fm'). In contrast, expression of proteins associated with Calvin - Benso n cycle (Rls, ativase RBC) and rubisco carboxylation activity ( in vivo and in vitro ) were not altered in mutants under normal growth conditions . In HL, the expression of proteins related to photosynthesis was strongly repressed in all genotypes , as well as gas exchange parameters and Fv/Fm, the latter being strong indication of photoinhibition. Moreover, proteins related to photorespiration showed increased expression/activity in response to HL in NT and maintenance of already high levels in OsAPX1/2. In OsAPX1/2 t h e expression and activity of chloroplastic Cu/Zn - SOD showed a similar response exhibited by photorespiration - related proteins, although the activity of thylakoid APX has been greatly reduced, meaning deficiency in water - water cycle. Taken togeth er, these data demonstrate that induction of expression of proteins related PET in OsAPX1/2 plants may represent a compensatory mechanism for maintaining the photosynthetic activity levels similar to NT. Moreover, in HL, it is possible that the increased e xpression of photorespiration - related proteins in OsAPX1/2 acts as alternative electron sink, compensating the deficiency in the water - water cycle from these plants
Em regiÃes tropicais, onde existe alta incidÃncia luminosa, os elÃtrons podem se acumular na cadeia transportadora (PET) produzindo grandes quantidades de H 2 O 2 e outras ROS, que podem gerar fotodano e fotoinibiÃÃo. Para sobreviver a esse desafio, plantas desenvolveram vÃrios mecanismos de atenuaÃÃo do excesso de energia nos fotossistemas, alÃm de contar com uma eficiente ma quinaria de remoÃÃo do excesso de H 2 O 2 , da qual fazem parte as APX citosÃlicas (cAPX). Entretanto, plantas duplamente silenciadas para as cAPX (OsAPX1/2) nÃo apresentam grandes diferenÃas morfo - fenotÃpicas quando comparadas Ãs nÃo transformadas (NT), embor a OsAPX1/2 apresente induÃÃo de expressÃo de diversas proteÃnas relacionadas com a fotossÃntese, comparadas com as NT. As implicaÃÃes fisiolÃgicas dessa induÃÃo, assim como suas consequÃncias para a resistÃncia de OsAPX1/2 contra estresses de alta luz (HL) , ainda sÃo pouco conhecidas. Objetivando clarificar o papel das cAPx na fotossÃntese, plantas de arroz OsAPX1/2 foram produzidas, submetidas a 24 horas de HL (2000 μ mol m - 2 s - 1 ) e estudadas quanto à expressÃo e atividade de proteÃnas relacionadas com a fotossÃntese, fotorespiraÃÃo e homeostase redox. A quantidade de diversas proteÃnas da PET (Lhcb1, PsbO, PsbP, PsbQ, PSAC, PC, e FDX FNR), bem como teores de Chl e Pheo foram aum entadas em OsAPX1/2 em condiÃÃes normais de crescimento sem causar alteraÃÃes nos parÃmetros de atividade fotoquÃmica in vivo (Fv/Fm e Δ Fm/Fm'). Em contraste, as proteÃnas relacionadas com expressÃo ciclo de Calvin - Benson (Rls, ativase de Rbc) e a ativida de de carboxilaÃÃo da rubisco ( in vivo e in vitro ) nÃo foram alterados nos mutantes em condiÃÃes normais de crescimento. Em HL, a expressÃo de proteÃnas relacionadas com fotossÃntese foi fortemente reprimida em ambos os genÃtipos, assim como os parÃmetros de trocas gasosas e Fv/Fm, sendo esse Ãltimo forte indÃcio de fotoinibiÃÃo. Por outro lado, as proteÃnas relacionadas com a fotorespiraÃÃo, ou mostraram aumento na expressÃo/atividade em resposta à luz elevada (NT) ou manutenÃÃo de nÃveis jà elevados (OsAP X1/2) . A expressÃo e atividade de Cu/Zn - SOD de cloroplastos mostrou resposta similar a exibida pelas proteÃnas da fotorespiraÃÃo, embora a atividade de APX de tilacÃides tenha sido fortemente reduzida em OsAPX1/2, evidenciando deficiÃncia no ciclo Ãgua - Ãgu a. Tomados em conjunto, estes dados demonstram que a induÃÃo da expressÃo de proteÃnas relacionadas com o PET em OsAPX1/2 pode representar um mecanismo compensatÃrio para a manutenÃÃo da atividade fotossintÃtica aos nÃveis da NT. Por outro lado, sob HL, à possÃvel que o aumento da expressÃo de proteÃnas associadas com fotorespira ÃÃo em OsAPX1/2 atue como dissipador alternativo de elÃtrons, compensando a deficiÃncia no ciclo da Ãgua - Ãgua dessas plantas
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Efanov, Alexander. "Stimulation of insulin secretion independently from changes in cytosolic free Ca²⁺-concentration : studies with imidazolines and inositol polyphosphates /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3876-8/.

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Lu, Ming. "Cardiac Energetics in the Isolated Heart by NMR Spectroscopy and Mathematical Modeling." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1270221813.

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Mhamdi, Amna. "Cytosolic enzymes involverd in NADP+ and glutathione reduction : roles in H2 O2 metabolism and signaling in arabidopsis." Paris 11, 2010. http://www.theses.fr/2010PA112167.

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L’augmentation de la disponibilité des espèces actives de l’oxygène, comme le H2 O2 est une caractéristique commune aux réponses aux stress biotiques et abiotiques. L’accumulation du H2 O2 est contrôlée par les catalases ou par les peroxydases. Ces derniers systèmes dépendent des réducteurs cellulaires comme l’ascorbate et le glutathion, dont les teneurs sont soutenues par le NADPH. Le flux augmenté via ces voies peut provoquer des perturbations (comme celles qui peuvent affecter le statut thiol-disulfure) qui prennent le relais pour la transduction des signaux oxydatifs. Bien que plusieurs enzymes puissent réguler le système NADPH-glutathion dans le cytosol, l’importance physiologique de chacune de ses enzymes reste à élucider. Cette étude est basée sur la combinaison d’approches génétiques, biochimiques, transcriptomiques et métaboliques dans le but d’analyser les rôles de la glutathion réductase cytosolique (GRI) et des déshydrogénases NADP-dépendantes dans le métabolisme, les réponses induites par le H2 O2 et la résistance aux pathogènes. L’analyse comparative des mutants T-ADN des trois catalases d'Arabidopsis a révélé que seulement cat2 montre des perturbations redox et un stress oxydatif conditionnel au niveau foliaire. Cette lignée a été donc utilisée comme un fond génétique pour examiner l'importance du système NADPH-glutathion cytosoliquedans la réponse au H₂ O₂ produit au niveau intracellulaire par une voie physiologiquement pertinente (la photorespiration). L'analyse comparative des mutants gr1, cat2 e(t cat2 gr1 a révélée que GR1 joue un rôle déterminant dans les réponses des feilles au H₂ O₂intracellulaire et qu'elle asure une expression génique appropriée via les voies de signalisation par l'acide salicylique (AS) et par l'acide jasmonique. Une strtégie similaire a été utilisée pour explorer les fonctions de l'isocitrate déshydrogène cytosolique à NADP (ICDH) et des deux glucose-6-phosphate déshydrogénases cytosoliques (G6PPD5 et G6PD6). Cette analyse a montré que ces trois enzymes contribuent au maintient du statut glutathion dans le fond cat2. L'étude a aussi révélée que la mutation icdh et les mutations g6pd produisent des effets distincts où antagonistes par rapport à la mort cellulaire déclenchée par H2 O2 aux réponses aux pathogènes SA dépendantes et à la résistance aux bactéries. Ainsi, l'étude montre que la GR ne peut être remplacée par la deuxième GR ou par le système thiorédoxine dans les conditions de sur-disponibilité de H2 O2 et met en évidence les fonctions spécifiques des systèmes cytosoliques producteurs de NADPH dans la détermination des résultantes du stress oxdatif
Increased availability of ractive oxygen species asuch as H2 O2 is a feature of biotic and abiotic stresses. H2 O2 accumulation is controlld either by catalases or by peroxidases. The second depend on cellular reductants such as ascorbate and glutathione, both of which are supported by NADPH pools. Increased flux through these pools may cause perturbations (eg. In thiol-disulfide statud) that act in the relay of H2 O2-dependent redox signals. Although several enzyme systems are known that could regulate the NADPH-glutathione system in the cytosoln the significance of each remians largely unknown. This study look a combined genetic, biochemicaln and transcript and metablotie profiling approach to analyzing the roles of cytosolic glutathione reductase (GR) and NADP-dependent dehydrogenases in metabolism, H2 O2-triggered responses, and biotic stress. Comparative analysis of T-DNA mutants for the three Arabidopsis catalases revealed that only cat2 showed conditional redox pertubation and stress in rosettes. This line was therefore used as a gnentic background to investigate the importance of the cytosolic NADPH-glutathione system in response to H₂ O₂ produced intracellularly through a physiologically relevant pathway (photorespiration). Comparative analysis of gr1, cat2 and cat2 gr1 mutant lines revealed that GR1 plays a crucial role in leaf reponses to intracellular H2 O2 and is required to ensure appropriate gene expression throug both salicylic acid (SA) and jasmonic acid signaling pathways. Using a similar strategy, the functions of cytosolic NADP-isocitrate dehydrogenase (ICDH) an the two cytosolic glucose-6-phosphate dehydrogenases (G6PD5 and G6PD6) were explored. This analysis provided evidence that all three dehydrogenases contribuate to maintaining glutathione status under conditions of increased H₂ O₂ availability but revealed that the icdh and g6pd mutations produce distinct or opposing effects on H2 O2-triggered cell death, SA-dependent pathogenesis reponses and bacterial resistance. Thus, the study shows that GRI cannot be replaced by the second GR or by the thioredoxin system under conditions of increased H2 O2 and provides evidence for the specificity of cytosolic NADPH-producing systems in determining the outcome of oxidative stress
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Silvers, Kimberly Jane. "The role of cytochrome P450-mediated C-oxidation and cytosolic nitroreduction in the metabolism, DNA binding, and mutagenicity of 1-nitropyrene in human liver." Case Western Reserve University School of Graduate Studies / OhioLINK, 1995. http://rave.ohiolink.edu/etdc/view?acc_num=case1062512189.

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Books on the topic "Metabolism; Cytosol"

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Curtis, William, Martin Kemper, Alexandra Miller, Robert Pawlosky, M. Todd King, and Richard L. Veech. Mitigation of Damage from Reactive Oxygen Species and Ionizing Radiation by Ketone Body Esters. Edited by Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0027.

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Reactive oxygen and nitrogen species, ROS and RNS, are ubiquitous in living cells. They have beneficial effects but are also the cause of a wide variety of diseases. However adding excessive amounts of reducing agents has a long history of clinical failure. This problem can be overcome by providing a novel ester of D-beta-hydroxybutyrate–R-1,3-butanediol, which is rapidly hydrolyzed to ketone bodies, the metabolism of which leads to the production of NADPH. The free cytosolic [NADP+]/[NADPH] redox potential is the most negative in the cell and sets the potential of the glutathione and ascorbic acid couples. Ketone bodies also act by inhibiting histone deacetylases, activating the transcription factor FOXO3 and increasing the transcription of enzymes involved in the destruction of ROS. Ketone esters would be effective in the treatment of a variety of disparate diseases where ROS play a role, ranging from Parkinson’s disease to radiation sickness and aging.
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Book chapters on the topic "Metabolism; Cytosol"

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Itoh, Roichi, Jun Oka, and Hisashi Ozasa. "Regulation of the Cytosol 5′-Nucleotidase of the Heart by Adenylate Energy Charge." In Purine and Pyrimidine Metabolism in Man V, 299–303. New York, NY: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-1248-2_47.

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Emes, Mike J., Ian J. Tetlow, and Caroline G. Bowsher. "Integration of metabolism within non-photosynthetic plastids, and with the cytosol." In Regulation of Primary Metabolic Pathways in Plants, 117–36. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4818-4_6.

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Hostetler, Karl Y., and Elisabeth J. Jellison. "Role of phospholipases in myocardial ischemia: effect of cardioprotective agents on the phospholipases A of heart cytosol and sarcoplasmic reticulum in vitro." In Lipid Metabolism in Normoxic and Ischemic Heart, 77–82. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1611-4_12.

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Nishinaka, Tohru, Tomoyuki Terada, Toshifumi Umemura, Hirofumi Nanjo, Tadashi Mizoguchi, and Tsutomu Nishihara. "Study on Dihydrodiol Dehydrogenase (I) Molecular Forms of the Enzyme and the Presence of a Dihydrodiol Specific Enzyme in Bovine Liver Cytosol." In Enzymology and Molecular Biology of Carbonyl Metabolism 3, 165–75. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5901-2_19.

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Lemasters, John J., Anna-Liisa Nieminen, Gregory J. Gores, Barnaby E. Wray, and Brian Herman. "Cytosolic Free Calcium and Cell Injury in Hepatocytes." In Cell Calcium Metabolism, 463–70. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5598-4_48.

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Williams, John P., Mobashsher U. Khan, and Doris Wong. "Temperature Regulation of Desaturation of Fatty Acids in Cytosolic and Chloroplastic Glycerolipids." In Plant Lipid Metabolism, 372–77. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-015-8394-7_101.

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Paul, Richard J. "Smooth Muscle Energy Metabolism: Cytosolic Compartmentation of Metabolism and Function." In Advances in Physiological Research, 295–304. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4615-9492-5_16.

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Hansford, Richard G., Rafael Moreno-Sánchez, and James M. Staddon. "Regulation of Pyruvate Dehydrogenase in Isolated Cardiac Myocytes and Hepatocytes by Cytosolic Calcium." In Cell Calcium Metabolism, 331–41. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5598-4_36.

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Lakatta, Edward G., Maurizio C. Capogrossi, Harold A. Spurgeon, and Michael D. Stern. "Characteristics and Functional Implications of Spontaneous Sarcoplasmic Reticulum-Generated Cytosolic Calcium Oscillations in Myocardial Tissue." In Cell Calcium Metabolism, 529–43. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5598-4_55.

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Nalbone, Gilles, Karl Y. Hostetler, Jeannie Leonardi, and Huguette Lafont. "Partial Characterization of the Cytosolic Phospholipase A1 of Rat Heart." In Enzymes of Lipid Metabolism II, 153–57. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5212-9_22.

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Conference papers on the topic "Metabolism; Cytosol"

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Jiang, Lei, Alexander Shestov, Lance S. Terada, Nicholas D. Adams, Michael T. McCabe, Beth Pietrak, Stan J. Schimidt, Benjamin Schwartz, and Ralph J. DeBerardinis. "Abstract A35: Cytosolic reductive carboxylation is required for mitochondrial redox homeostasis during anchorage-independent cell growth." In Abstracts: AACR Special Conference: Metabolism and Cancer; June 7-10, 2015; Bellevue, WA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.metca15-a35.

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Holmsen, Holm, Ole-Bjørn Tysnes, Adrie J. M. Verhoeven, Vidar M. Steen, Lindsey J. Moore, and Sissel Rongved. "INHIBITION BY NEOMYCIN OF AGONIST-INDUCED POLYPHOSPHOINOSITIDE METABOLISM AND RESPONSES IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644521.

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Signal processing in platelets seems to involve polyphosphoinositide (PPI) metabolism, although direct coupling between PPI metabolism and responses has not been proved. Neomycin binds tightly to PPIs and has been used to probe the involvement of PPI metabolism and responses in platelets. Neomycin(SO4)3 powerfully inhibited ADP- and adrenaline-induced aggregation of platelets in PRP. This was partly due to the sulphate anion; the chloride form was therefore prepared. Platelets were prelabelled in PRP with 32P-Pi. and transferred by gel filtration to a calcium-free Tyrode’s solution (GFP). Increasing concentrations (2-5 mM) of neomycinCl6 caused progressive inhibition of thrombin-induced aggregation, dense granule secretion, acid hydrolase secretion and formation of 32P-phosphatidic acid (PA); the inhibition was immediate, not affected by aspirin and counteracted by increasing thrombin concentrations. Incubation of neomycin (up to 5 mM) with this GFP or with P-Pi. On GFP prepared from unlabelled PRP had no effect on the P content of ATP, phosphatidylinositol-4-phosphate (PIP) or phosphatidylinositol-4,5-bisphosphate (PIP ). Increasing neomycin concentrations caused progressive inhibition of the thrombin-induced init^l (10 sec) decrease, but not of the late (90 sec) incg^ase i-n P-PIP2 while they enhanced the increase in P-PIP. Similar results were obtained ^th collagen and PAF. Both the increase in cytosolic Ca and pH (measured by INDO-I and BCECF, respectively) induced by thrombin were inhibited progressively by increasing concentrations of neomycin. These results are in support for a direct involvement of PPI metabolism in the stimulus-response coupling below the receptor level. However, the failure of neomycin to affect turnover of PIP and PIP2 in nonstimulated platelets suggests that the aminoglycoside does not penetrate the membrane, and only become available to PPI during stimulation.
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Rao, G. H. R., J. M. Gerrard, and J. G. White. "EPINEPHRINE INDUCED POTENTIATION OF ARACHIDONATE AGGREGATION IN OUIN 2 LOADED PLATELETS IS NOT MEDIATED BY ELEVATION OF CYTOSOLIC CALCIUM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643761.

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Previous studies have demonstrated that chelation of ionized cytosolic calcium by Ouin 2 leads to a refractory state in platelets.However, epinephrine (Epi) induced membranemodulation restored the sensitivity of Ouin 2loaded platelets to the action of agonists.Further studies with Ouin 2 and Fura 2 suggested that Epi induced recovery of sensitivity by refractory platelets to aggregation by arachidonate does not require elevation of cytosolic calcium. To further delineate the role of calcium in membrane modulation, we followed phosphoinositol metabolism and myosinlight chain phosphorylation using radiolabeled platelets. The total amount of PI metabolites generated after exposure to Epi, AA or Epi + AA were significantly less than that formed after 0.1 μ thrombin stimulation. Ouin 2 at 40 μM concentration had no inhibitory effect on PI hydrolysis. However, at this concentration it effectively blocked AA induced aggregation. Although Epi treatment restored the sensitivity of Ouin 2 loaded platelets to the action of AA, it did not enhance the formation of increased quantitites of PI metabolites. Similar to earlierstudies, Ouin 2 loading effectively blocked phosphorylation of myosin light chain (20 K).Although a combination of Epi + AA restoredsome phosphorylation of 20 K protein in Ouin2 loaded platelets, the degree of phosphorylation was significantly less than that achieved in control stimulated platelets. Resultsof these studies suggest that Epi induced restoration of sensitivity to refractory, Ouin2 loaded platelets is not mediated by 1) significant elevation of cytosolic calcium, 2) enhanced production of PI metabolites, 3) increased phosphorylation of 20 K protein. Epiinduced membrane modulation is a novel, independent mechanism capable of restoring sensitivity to agonists in platelets with compromised function.
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Koutouzov, S., A. Remmal, P. Marche, and P. Meyer. "IMPAIRMENT OF PLATELET PHOSPHOINOSITIDE METABOLISM IN PRIMARY HYPERTENSION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643812.

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Blood platelets from hypertensive patients and spontaneously hypertensive rats (SHR) display multiple abnormalities when compared with cells from normotensive controls. The major features of the modified platelet profile are an enhanced rate of adhesion/aggregation in response to many stimuli, a greater sensitivity for thrombin and adrenaline to produce increases in cytoplasmic free Ca2+, and an exaggerated release reaction. Furthermore, the resting levels of cytosolic free Ca2+ ions are specifically and constantly increased. Since phosphoinositides are involved in the stimulus-response coupling mediated by intracellular Ca2+ mobilization, the metabolism of these lipids was investigated in platelets of SHR and compared with those of normotensive Wistar-Kyoto rats (WKY). Following 32P-labelling of quiescent platelets, labeled lipids were analyzed both in platelets at rest and after thrombin stimulation. In resting platelets, the 32P associated with each of the phosphoinositides and phosphatidic acid (PA) was similar in SHR and WKY indicating that both the pool size of the various lipids and their basal turnover did not differ between the two strains. By contrast, within the first seconds after thrombin stimulation (10-60 sec), the dose-response and time-course curves of agonist-induced increase in 32P-PA were markedly shifted to the left and reached higher equilibrium levels in SHR. Since thrombin-induced 32P-PA formation is held as the most sensitive index of phospholipase C activity, our results indicate that this enzyme displays hyperreactivity in SHR (vs WKY). It is therefore likely that in SHR, the enhanced physiological responses (serotonin secretion, aggregation) that we observed under the same experimental conditions may be related to an increased formation of Phospholipase C products (inosi-toltriphosphate and diacylglycerol) which are the two second messengers responsible for internal Ca2+ mobilization and activation of protein kinase C, respectively. Therefore, these data suggest that the hypersensitivity of Phospholipase C may be involved in the overall alteration of cell calcium handling and hence in the SHR platelet responses.
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Wallace-Povirk, Adrianne, Carrie O’Connor, Aamod Dekhne, Zhanjun Hou, Md Junayed Nayeen, Khushbu Shah, Aleem Gangjee, and Larry Matherly. "Abstract 4800: Targeting mitochondrial and cytosolic one-carbon metabolism in epithelial ovarian cancer via folate receptor alpha." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4800.

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Wallace-Povirk, Adrianne, Carrie O’Connor, Aamod Dekhne, Zhanjun Hou, Md Junayed Nayeen, Khushbu Shah, Aleem Gangjee, and Larry Matherly. "Abstract 4800: Targeting mitochondrial and cytosolic one-carbon metabolism in epithelial ovarian cancer via folate receptor alpha." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4800.

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Wallace-Povirk, Adrianne C., Carrie O'Connor, Xun Bao, Jade Katinas, Jennifer Wong-Roushar, Aamod Dekhne, Zhanjun Hou, et al. "Abstract 2348: Targeting mitochondrial and cytosolic one-carbon metabolism in epithelial ovarian cancer via folate receptor alpha." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2348.

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Papathanassiu, Adonia E., and Hong A. Vu. "Abstract 3216: Cytosolic leucine metabolism regulates the expression of prometastatic proteins: The genesis of a new druggable target." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3216.

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BLACHE, D., and M. CIAVATTI. "ARACHIDONATE METABOLISM IN RAT PLATELETS IN THE PRESENCE OF Ca2+-SUBSTITUTES (Sr2+, BA2+)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643392.

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To further document the involvement of external Ca2+ in the platelet induced-activation process, we have studied the arachidonate (AA) metabolism of intact washed rat platelets in the presence of different concentrations of Ca2+, Sr2+ or Ba2+. The thrombin-induced mobilization of [3H]- or [14C]-AA preincorporated into platelet phospholipids was followed as well as the subsequent formation of labeled cyclooxygenase and lipoxygenase products (CLP). Results indicate that upon thrombin (<0.1 U/ml) stimulation, AA release and CLP formation are reduced by 50 to 90% only by omission of Ca2+ as compared to 1 mM Ca2+ in the suspending medium. In higher Ca2+ concentrations (5 mM), the AA mobilization and CLP formation are inhibited and the data are close to those obtained in the absence of Ca2+. In the presence of Sr2+ or Ba2+, results indicate that these cations can substitute to Ca2+. Similarly to Ca2+, an optimum concentration is found in Sr2+ or Ba2+ (3-5 mM) and higher concentrations inhibit AA release and CLP formation.We have also studied the activity of a semi-purified preparation of phospholipase A2 (PLA2) from rat platelets. This activity was assayed (pH 9) using heat-denaturated (3H)-AA prelabeled phospholipids as substrate. The results show that this PLA2 activity was strongly Ca2+-dependent. We found that unlike Mg2+, Sr2+ and Ba2+ are able to greatly enhance this activity. Relative effiency (Vmax) are in the order Ca2+>Sr2+>Ba2+. Taken together, these findings as well as our previous results (Blache et al, BBA 1987, in press) suggest that external Ca2+ may play a major role in the regulation of rat platelet activity. Our interpretation is in line with the view that Sr2+ or Ba2+ could enter the platelet through a mechanism common to Ca2+ (a kind of Ca2+ channel). Although direct evidence await the results of further studies which are in progress, it can be considered that Sr2+ or Ba2+ might cause platelet induced-activation mimickigci a rise in the cytosolic Ca2+ and subsequent activation of Ca2+-dependent enzymes.
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Kienast, J., J. Arnout, G. Pfliegler, H. Deckmyn, B. Hoet, and J. Vermylen. "DISSOCIATION OF PHOSPHOLIPASE A2 ACTIVATION FROM CYTOSOLIC FREE CA2+ MOBILIZATION IN PLATELETS EXPOSED TO FLUORIDE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644529.

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Elevated cytosolic free Ca2+ concentrations ([Ca2+]i) are thought to be required for phosphol ipase A2 activity to liberate arachidonic acid (AA) from membrane phospholipids in platelets. The major AA metabolite formed during agonist-induced platelet activation is thromboxane A2 (TxA2). We have investigated the effect of sodium fluoride (NaF) on platelet TxAz formation in correlation to platelet functional changes (aggregation and release of ATP) and intracellular events specific for either agonist- or antagonist-induced platelet responses. A first peak in platelet TxAffi formation reaching 30 × control values was observed at 20 - 30 mM of NaF which also induced platelet aggregation and release of ATP in association with a rise in [Ca2+]i . Increasing the concentration of NaF resulted in a decrease in TxA2 release to a minimum of 12 × control values at 50 mM. A second, concentration-dependent rise in TxA2 formation was observed at higher concentrations of NaF with a maximum of 40 × control values at 100 mM. These concentrations, however, did induce neither aggregation nor a significant rise in [Ca2+]i but a rapid, transient increase in platelet cAMP levels. Activation of phospholipase C and protein kinase C was observed at all concentrations of NaF tested whereby the rate rather than the extent of activation of these enzymes was concentration-dependent. Our results demonstrate that fluoride at high concentrations can induce platelet TxA2 formation in the absence of elevated [Ca2+]i suggesting an additional, Ca2+-independent mechanism of phospholipase A2 activation possibly mediated by fluoride sensitive GTP-binding regulatory proteins.
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