Base de dados : MEDLINE
Pesquisa : G02.111.833 [Categoria DeCS]
Referências encontradas : 138 [refinar]
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  1 / 138 MEDLINE  
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[PMID]:27077116
[Au] Autor:Zhang Y; Li C; Li H; Song Y; Zhao Y; Zhai L; Wang H; Zhong R; Tang H; Zhu D
[Ad] Endereço:The State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and School of Basic Medicine, Peking Union Medical College, Beijing 100005, PR China.
[Ti] Título:miR-378 Activates the Pyruvate-PEP Futile Cycle and Enhances Lipolysis to Ameliorate Obesity in Mice.
[So] Source:EBioMedicine;5:93-104, 2016 Mar.
[Is] ISSN:2352-3964
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Obesity has been linked to many health problems, such as diabetes. However, there is no drug that effectively treats obesity. Here, we reveal that miR-378 transgenic mice display reduced fat mass, enhanced lipolysis, and increased energy expenditure. Notably, administering AgomiR-378 prevents and ameliorates obesity in mice. We also found that the energy deficiency seen in miR-378 transgenic mice was due to impaired glucose metabolism. This impairment was caused by an activated pyruvate-PEP futile cycle via the miR-378-Akt1-FoxO1-PEPCK pathway in skeletal muscle and enhanced lipolysis in adipose tissues mediated by miR-378-SCD1. Our findings demonstrate that activating the pyruvate-PEP futile cycle in skeletal muscle is the primary cause of elevated lipolysis in adipose tissues of miR-378 transgenic mice, and it helps orchestrate the crosstalk between muscle and fat to control energy homeostasis in mice. Thus, miR-378 may serve as a promising agent for preventing and treating obesity in humans.
[Mh] Termos MeSH primário: Metabolismo Energético/genética
MicroRNAs/genética
Obesidade/genética
Ciclização de Substratos/genética
[Mh] Termos MeSH secundário: Tecido Adiposo/metabolismo
Animais
Dieta Hiperlipídica
Glucose/metabolismo
Seres Humanos
Lipólise/genética
Camundongos
Camundongos Transgênicos
MicroRNAs/administração & dosagem
Músculo Esquelético/metabolismo
Músculo Esquelético/patologia
Obesidade/patologia
Obesidade/terapia
Oligorribonucleotídeos/administração & dosagem
Oligorribonucleotídeos/genética
Ácido Pirúvico/metabolismo
Termogênese
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (MIRN378 microRNA, mouse); 0 (MicroRNAs); 0 (Oligoribonucleotides); 8558G7RUTR (Pyruvic Acid); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161231
[Lr] Data última revisão:
161231
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160415
[St] Status:MEDLINE
[do] DOI:10.1016/j.ebiom.2016.01.035


  2 / 138 MEDLINE  
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[PMID]:26890808
[Au] Autor:Semkiv MV; Dmytruk KV; Abbas CA; Sibirny AA
[Ad] Endereço:a Institute of Cell Biology, NAS of Ukraine , Lviv , Ukraine.
[Ti] Título:Activation of futile cycles as an approach to increase ethanol yield during glucose fermentation in Saccharomyces cerevisiae.
[So] Source:Bioengineered;7(2):106-11, 2016 Apr 02.
[Is] ISSN:2165-5987
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:An increase in ethanol yield by yeast from the fermentation of conventional sugars such as glucose and sucrose is possible by reducing the production of a key byproduct such as cellular biomass. Previously we have reported that overexpression of PHO8 gene encoding non-specific ATP-hydrolyzing alkaline phosphatase can lead to a decrease in cellular ATP content and to an increase in ethanol yield during glucose fermentation by Saccharomyces cerevisiae. In this work we further report on 2 new successful approaches to reduce cellular levels of ATP that increase ethanol yield and productivity. The first approach is based on the overexpression of the heterologous Escherichia coli apy gene encoding apyrase or SSB1 part of the chaperon that exhibit ATPase activity in yeast. In the second approach we constructed a futile cycle by the overexpression of S. cerevisiae genes encoding pyruvate carboxylase and phosphoenolpyruvate carboxykinase in S. cerevisiae. These genetically engineered strains accumulated more ethanol compared to the wild-type strain during alcoholic fermentation.
[Mh] Termos MeSH primário: Fermentação
Saccharomyces cerevisiae/genética
[Mh] Termos MeSH secundário: Etanol
Glucose
Ciclização de Substratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
3K9958V90M (Ethanol); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160219
[St] Status:MEDLINE
[do] DOI:10.1080/21655979.2016.1148223


  3 / 138 MEDLINE  
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[PMID]:26578677
[Au] Autor:Mok WW; Park JO; Rabinowitz JD; Brynildsen MP
[Ad] Endereço:Department of Chemical and Biological Engineering, Princeton University, Princeton, New Jersey, USA.
[Ti] Título:RNA Futile Cycling in Model Persisters Derived from MazF Accumulation.
[So] Source:MBio;6(6):e01588-15, 2015 Nov 17.
[Is] ISSN:2150-7511
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Metabolism plays an important role in the persister phenotype, as evidenced by the number of strategies that perturb metabolism to sabotage this troublesome subpopulation. However, the absence of techniques to isolate high-purity populations of native persisters has precluded direct measurement of persister metabolism. To address this technical challenge, we studied Escherichia coli populations whose growth had been inhibited by the accumulation of the MazF toxin, which catalyzes RNA cleavage, as a model system for persistence. Using chromosomally integrated, orthogonally inducible promoters to express MazF and its antitoxin MazE, bacterial populations that were almost entirely tolerant to fluoroquinolone and ß-lactam antibiotics were obtained upon MazF accumulation, and these were subjected to direct metabolic measurements. While MazF model persisters were nonreplicative, they maintained substantial oxygen and glucose consumption. Metabolomic analysis revealed accumulation of all four ribonucleotide monophosphates (NMPs). These results are consistent with a MazF-catalyzed RNA futile cycle, where the energy derived from catabolism is dissipated through continuous transcription and MazF-mediated RNA degradation. When transcription was inhibited, oxygen consumption and glucose uptake decreased, and nucleotide triphosphates (NTPs) and NTP/NMP ratios increased. Interestingly, the MazF-inhibited cells were sensitive to aminoglycosides, and this sensitivity was blocked by inhibition of transcription. Thus, in MazF model persisters, futile cycles of RNA synthesis and degradation result in both significant metabolic demands and aminoglycoside sensitivity. IMPORTANCE: Metabolism plays a critical role in controlling each stage of bacterial persistence (shutdown, stasis, and reawakening). In this work, we generated an E. coli strain in which the MazE antitoxin and MazF toxin were artificially and independently inducible, and we used this strain to generate model persisters and study their metabolism. We found that even though growth of the model persisters was inhibited, they remained highly metabolically active. We further uncovered a futile cycle driven by continued transcription and MazF-mediated transcript degradation that dissipated the energy derived from carbon catabolism. Interestingly, the existence of this futile cycle acted as an Achilles' heel for MazF model persisters, rendering them vulnerable to killing by aminoglycosides.
[Mh] Termos MeSH primário: Proteínas de Ligação a DNA/metabolismo
Endorribonucleases/metabolismo
Proteínas de Escherichia coli/metabolismo
Escherichia coli/enzimologia
RNA Bacteriano/metabolismo
[Mh] Termos MeSH secundário: Antibacterianos/farmacologia
Proteínas de Ligação a DNA/genética
Tolerância a Medicamentos
Endorribonucleases/genética
Escherichia coli/efeitos dos fármacos
Escherichia coli/metabolismo
Proteínas de Escherichia coli/genética
Fluoroquinolonas/farmacologia
Expressão Gênica
Glucose/metabolismo
Oxigênio/metabolismo
Regiões Promotoras Genéticas
Estabilidade de RNA
Ribonucleotídeos/metabolismo
Ciclização de Substratos
Transcrição Genética
beta-Lactamas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (DNA-Binding Proteins); 0 (Escherichia coli Proteins); 0 (Fluoroquinolones); 0 (MazE protein, E coli); 0 (MazF protein, E coli); 0 (RNA, Bacterial); 0 (Ribonucleotides); 0 (beta-Lactams); EC 3.1.- (Endoribonucleases); IY9XDZ35W2 (Glucose); S88TT14065 (Oxygen)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151119
[St] Status:MEDLINE


  4 / 138 MEDLINE  
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[PMID]:25899755
[Au] Autor:Hädicke O; Bettenbrock K; Klamt S
[Ad] Endereço:Max Planck Institute for Dynamics of Complex Technical Systems1Sandtorstrasse 1, Magdeburg 39106, Germany.
[Ti] Título:Enforced ATP futile cycling increases specific productivity and yield of anaerobic lactate production in Escherichia coli.
[So] Source:Biotechnol Bioeng;112(10):2195-9, 2015 Oct.
[Is] ISSN:1097-0290
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The manipulation of cofactor pools such as ATP or NAD(P)H has for long been recognized as key targets for metabolic engineering of microorganisms to improve yields and productivities of biotechnological processes. Several works in the past have shown that enforcing ATP futile cycling may enhance the synthesis of certain products under aerobic conditions. However, case studies demonstrating that ATP wasting may also have beneficial effects for anaerobic production processes are scarce. Taking lactic acid as an economically relevant product, we demonstrate that induction of ATP futile cycling in Escherichia coli leads to increased yields and specific production rates under anaerobic conditions, even in the case where lactate is already produced with high yields. Specifically, we constructed a high lactate producer strain KBM10111 (= MG1655 ΔadhE::Cam ΔackA-pta) and implemented an IPTG-inducible overexpression of ppsA encoding for PEP synthase which, together with pyruvate kinase, gives rise to an ATP consuming cycle. Under induction of ppsA, KBM10111 exhibits a 25% higher specific lactate productivity as well as an 8% higher lactate yield. Furthermore, the specific substrate uptake rate was increased by 14%. However, trade-offs between specific and volumetric productivities must be considered when ATP wasting strategies are used to shift substrate conversion from biomass to product synthesis and we discuss potential solutions to design optimal processes. In summary, enforced ATP futile cycling has great potential to optimize a variety of production processes and our study demonstrates that this holds true also for anaerobic processes.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/metabolismo
Escherichia coli/genética
Escherichia coli/metabolismo
Ácido Láctico/metabolismo
Engenharia Metabólica/métodos
Ciclização de Substratos
[Mh] Termos MeSH secundário: Anaerobiose
Deleção de Genes
Mutagênese Insercional
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
33X04XA5AT (Lactic Acid); 8L70Q75FXE (Adenosine Triphosphate)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:150826
[Lr] Data última revisão:
150826
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150423
[St] Status:MEDLINE
[do] DOI:10.1002/bit.25623


  5 / 138 MEDLINE  
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[PMID]:25732623
[Au] Autor:Adolfsen KJ; Brynildsen MP
[Ad] Endereço:Department of Chemical and Biological Engineering, Princeton University, Princeton, NJ 08544, United States. Electronic address: adolfsen@princeton.edu.
[Ti] Título:Futile cycling increases sensitivity toward oxidative stress in Escherichia coli.
[So] Source:Metab Eng;29:26-35, 2015 May.
[Is] ISSN:1096-7184
[Cp] País de publicação:Belgium
[La] Idioma:eng
[Ab] Resumo:Reactive oxygen species (ROS) are toxic molecules utilized by the immune system to combat invading pathogens. Recent evidence suggests that inefficiencies in ATP production or usage can lead to increased endogenous ROS production and sensitivity to oxidative stress in bacteria. With this as inspiration, and knowledge that ATP is required for a number of DNA repair mechanisms, we hypothesized that futile cycling would be an effective way to increase sensitivity to oxidative stress. We developed a mixed integer linear optimization framework to identify experimentally-tractable futile cycles, and confirmed metabolic modeling predictions that futile cycling depresses growth rate, and increases both O2 consumption and ROS production per biomass generated. Further, intracellular ATP was decreased and sensitivity to oxidative stress increased in all actively cycling strains compared to their catalytically inactive controls. This research establishes a fundamental connection between ATP metabolism, endogenous ROS production, and tolerance toward oxidative stress in bacteria.
[Mh] Termos MeSH primário: Escherichia coli K12/metabolismo
Estresse Oxidativo/fisiologia
Espécies Reativas de Oxigênio/metabolismo
Ciclização de Substratos/fisiologia
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/genética
Trifosfato de Adenosina/metabolismo
Reparo do DNA/fisiologia
Escherichia coli K12/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Reactive Oxygen Species); 8L70Q75FXE (Adenosine Triphosphate)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150304
[St] Status:MEDLINE


  6 / 138 MEDLINE  
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[PMID]:24945955
[Au] Autor:Nikiforova AB; Saris NE; Kruglov AG
[Ad] Endereço:Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, 142290 Pushchino, Moscow Region, Russia.
[Ti] Título:External mitochondrial NADH-dependent reductase of redox cyclers: VDAC1 or Cyb5R3?
[So] Source:Free Radic Biol Med;74:74-84, 2014 Sep.
[Is] ISSN:1873-4596
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It was reported that VDAC1 possesses an NADH oxidoreductase activity and plays an important role in the activation of xenobiotics in the outer mitochondrial membrane. In the present work, we evaluated the participation of VDAC1 and Cyb5R3 in the NADH-dependent activation of various redox cyclers in mitochondria. We show that external NADH oxidoreductase caused the redox cycling of menadione ≫ lucigenin>nitrofurantoin. Paraquat was predominantly activated by internal mitochondria oxidoreductases. An increase in the ionic strength stimulated and suppressed the redox cycling of negatively and positively charged acceptors, as was expected for the Cyb5R3-mediated reduction. Antibodies against Cyb5R3 but not VDAC substantially inhibited the NADH-related oxidoreductase activities. The specific VDAC blockers G3139 and erastin, separately or in combination, in concentrations sufficient for the inhibition of substrate transport, exhibited minimal effects on the redox cycler-dependent NADH oxidation, ROS generation, and reduction of exogenous cytochrome c. In contrast, Cyb5R3 inhibitors (6-propyl-2-thiouracil, p-chloromercuriobenzoate, quercetin, mersalyl, and ebselen) showed similar patterns of inhibition of ROS generation and cytochrome c reduction. The analysis of the spectra of the endogenous cytochromes b5 and c in the presence of nitrofurantoin and the inhibitors of VDAC and Cyb5R3 demonstrated that the redox cycler can transfer electrons from Cyb5R3 to endogenous cytochrome c. This caused the oxidation of outer membrane-bound cytochrome b5, which is in redox balance with Cyb5R3. The data obtained argue against VDAC1 and in favor of Cyb5R3 involvement in the activation of redox cyclers in the outer mitochondrial membrane.
[Mh] Termos MeSH primário: Citocromo-B(5) Redutase/metabolismo
Mitocôndrias Hepáticas/metabolismo
Membranas Mitocondriais/metabolismo
Ciclização de Substratos
Canal de Ânion 1 Dependente de Voltagem/metabolismo
[Mh] Termos MeSH secundário: Animais
Citocromos c/metabolismo
Transporte de Elétrons
Masculino
NAD/metabolismo
Concentração Osmolar
Oxirredução
Paraquat/metabolismo
Ratos
Ratos Wistar
Xenobióticos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Xenobiotics); 0U46U6E8UK (NAD); 9007-43-6 (Cytochromes c); EC 1.6.- (Voltage-Dependent Anion Channel 1); EC 1.6.2.2 (Cytochrome-B(5) Reductase); EC 1.6.2.2 (Dia1 protein, rat); PLG39H7695 (Paraquat)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:140826
[Lr] Data última revisão:
140826
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140620
[St] Status:MEDLINE


  7 / 138 MEDLINE  
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[PMID]:24235282
[Au] Autor:Emmett M
[Ad] Endereço:Division of Nephrology, Department of Internal Medicine, Baylor University Medical Center, Dallas, Texas.
[Ti] Título:Acetaminophen toxicity and 5-oxoproline (pyroglutamic acid): a tale of two cycles, one an ATP-depleting futile cycle and the other a useful cycle.
[So] Source:Clin J Am Soc Nephrol;9(1):191-200, 2014 Jan.
[Is] ISSN:1555-905X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The acquired form of 5-oxoproline (pyroglutamic acid) metabolic acidosis was first described in 1989 and its relationship to chronic acetaminophen ingestion was proposed the next year. Since then, this cause of chronic anion gap metabolic acidosis has been increasingly recognized. Many cases go unrecognized because an assay for 5-oxoproline is not widely available. Most cases occur in malnourished, chronically ill women with a history of chronic acetaminophen ingestion. Acetaminophen levels are very rarely in the toxic range; rather, they are usually therapeutic or low. The disorder generally resolves with cessation of acetaminophen and administration of intravenous fluids. Methionine or N-acetyl cysteine may accelerate resolution and methionine is protective in a rodent model. The disorder has been attributed to glutathione depletion and activation of a key enzyme in the γ-glutamyl cycle. However, the specific metabolic derangements that cause the 5-oxoproline accumulation remain unclear. An ATP-depleting futile 5-oxoproline cycle can explain the accumulation of 5-oxoproline after chronic acetaminophen ingestion. This cycle is activated by the depletion of both glutathione and cysteine. This explanation contributes to our understanding of acetaminophen-induced 5-oxoproline metabolic acidosis and the beneficial role of N-acetyl cysteine therapy. The ATP-depleting futile 5-oxoproline cycle may also play a role in the energy depletions that occur in other acetaminophen-related toxic syndromes.
[Mh] Termos MeSH primário: Acetaminofen/envenenamento
Acidose/induzido quimicamente
Trifosfato de Adenosina/metabolismo
Analgésicos não Entorpecentes/envenenamento
Metabolismo Energético/efeitos dos fármacos
Ácido Pirrolidonocarboxílico/metabolismo
[Mh] Termos MeSH secundário: Acetaminofen/metabolismo
Equilíbrio Ácido-Base/efeitos dos fármacos
Acidose/metabolismo
Acidose/terapia
Analgésicos não Entorpecentes/metabolismo
Animais
Cisteína/deficiência
Glutationa/deficiência
Seres Humanos
Envenenamento/etiologia
Envenenamento/metabolismo
Prognóstico
Ciclização de Substratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Analgesics, Non-Narcotic); 362O9ITL9D (Acetaminophen); 8L70Q75FXE (Adenosine Triphosphate); GAN16C9B8O (Glutathione); K848JZ4886 (Cysteine); SZB83O1W42 (Pyrrolidonecarboxylic Acid)
[Em] Mês de entrada:1409
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131116
[St] Status:MEDLINE
[do] DOI:10.2215/CJN.07730713


  8 / 138 MEDLINE  
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[PMID]:24094413
[Au] Autor:Alam-Nazki A; Krishnan J
[Ad] Endereço:Centre for Process Systems Engineering, Department of Chemical Engineering, Imperial College London, London, UK.
[Ti] Título:Covalent modification cycles through the spatial prism.
[So] Source:Biophys J;105(7):1720-31, 2013 Oct 01.
[Is] ISSN:1542-0086
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Covalent modification cycles are basic units and building blocks of posttranslational modification and cellular signal transduction. We systematically explore different spatial aspects of signal transduction in covalent modification cycles by starting with a basic temporal cycle as a reference and focusing on steady-state signal transduction. We consider, in turn, the effect of diffusion on spatial signal transduction, spatial analogs of ultrasensitive behavior, and the interplay between enzyme localization and substrate diffusion. Our analysis reveals the need to explicitly account for kinetics and diffusional transport (and localization) of enzymes, substrates, and complexes. It demonstrates a complex and subtle interplay between spatial heterogeneity, diffusion, and localization. Overall, examining the spatial dimension of covalent modification reveals that 1), there are important differences between spatial and temporal signal transduction even in this cycle; and 2), spatial aspects may play a substantial role in affecting and distorting information transfer in modules/networks that are usually studied in purely temporal terms. This has important implications for the systematic understanding of signaling in covalent modification cycles, pathways, and networks in multiple cellular contexts.
[Mh] Termos MeSH primário: Modelos Biológicos
Transdução de Sinais
[Mh] Termos MeSH secundário: Difusão
Enzimas/metabolismo
Cinética
Processamento de Proteína Pós-Traducional
Ciclização de Substratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Enzymes)
[Em] Mês de entrada:1405
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131008
[St] Status:MEDLINE


  9 / 138 MEDLINE  
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[PMID]:23681571
[Au] Autor:Graeff RM; Lee HC
[Ad] Endereço:Department of Physiology, The University of Hong Kong, Hong Kong, China.
[Ti] Título:Determination of ADP-ribosyl cyclase activity, cyclic ADP-ribose, and nicotinic acid adenine dinucleotide phosphate in tissue extracts.
[So] Source:Methods Mol Biol;1016:39-56, 2013.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cyclic ADP-ribose (cADPR) is a novel second messenger that releases calcium from intracellular stores. Although first shown to release calcium in the sea urchin egg, cADPR has been shown since to be active in a variety of cells and tissues, from plant to human. cADPR stimulates calcium release via ryanodine receptors although the mechanism is still not completely understood. cADPR is produced enzymatically from NAD by ADP-ribosyl cyclases; several of these proteins have been identified including one isolated from Aplysia californica, two types found in mammals (CD38 and CD157), and three forms in sea urchin. A cyclase activity has been measured in extracts from Arabidopsis thaliana although the protein is still unidentified. Nicotinic acid adenine dinucleotide phosphate (NAADP) is another novel messenger that releases calcium from internal stores and is produced by these same enzymes by an exchange reaction. NAADP targets lysosomal stores whereas cADPR releases calcium from the endoplasmic reticulum. Due to their importance in cell signaling, cADPR and NAADP have been the focus of numerous investigations over the last 25 years. This chapter describes several assay methods for the measurements of cADPR and NAADP concentration and cyclase activity in extracts from cells.
[Mh] Termos MeSH primário: ADP-Ribosil Ciclase/metabolismo
ADP-Ribose Cíclica/metabolismo
NADP/análogos & derivados
Extratos de Tecidos/metabolismo
[Mh] Termos MeSH secundário: ADP-Ribosil Ciclase 1/metabolismo
Animais
Cromatografia Líquida de Alta Pressão
Fluorescência
Nucleotídeos de Guanina
Seres Humanos
NAD/análogos & derivados
NAD+ Nucleosidase/metabolismo
NADP/metabolismo
Ciclização de Substratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Guanine Nucleotides); 0 (Tissue Extracts); 0U46U6E8UK (NAD); 119340-53-3 (Cyclic ADP-Ribose); 53-59-8 (NADP); 5502-96-5 (NAADP); 5624-35-1 (nicotinamide guanine dinucleotide); EC 3.2.2.5 (ADP-ribosyl Cyclase); EC 3.2.2.5 (NAD+ Nucleosidase); EC 3.2.2.6 (ADP-ribosyl Cyclase 1)
[Em] Mês de entrada:1312
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130518
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-62703-441-8_4


  10 / 138 MEDLINE  
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[PMID]:23382859
[Au] Autor:Claeyssen E; Dorion S; Clendenning A; He JZ; Wally O; Chen J; Auslender EL; Moisan MC; Jolicoeur M; Rivoal J
[Ad] Endereço:Institut de Recherche en Biologie Végétale, Université de Montréal, Montréal, Québec, Canada.
[Ti] Título:The futile cycling of hexose phosphates could account for the fact that hexokinase exerts a high control on glucose phosphorylation but not on glycolytic rate in transgenic potato (Solanum tuberosum) roots.
[So] Source:PLoS One;8(1):e53898, 2013.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The metabolism of potato (Solanum tuberosum) roots constitutively over- and underexpressing hexokinase (HK, EC 2.7.1.1) was examined. An 11-fold variation in HK activity resulted in altered root growth, with antisense roots growing better than sense roots. Quantification of sugars, organic acids and amino acids in transgenic roots demonstrated that the manipulation of HK activity had very little effect on the intracellular pools of these metabolites. However, adenylate and free Pi levels were negatively affected by an increase in HK activity. The flux control coefficient of HK over the phosphorylation of glucose was measured for the first time in plants. Its value varied with HK level. It reached 1.71 at or below normal HK activity value and was much lower (0.32) at very high HK levels. Measurements of glycolytic flux and O(2) uptake rates demonstrated that the differences in glucose phosphorylation did not affect significantly glycolytic and respiratory metabolism. We hypothesized that these results could be explained by the existence of a futile cycle between the pools of hexose-Ps and carbohydrates. This view is supported by several lines of evidence. Firstly, activities of enzymes capable of catalyzing these reactions were detected in roots, including a hexose-P phosphatase. Secondly, metabolic tracer experiments using (14)C-glucose as precursor showed the formation of (14)C-fructose and (14)C-sucrose. We conclude that futile cycling of hexose-P could be partially responsible for the differences in energetic status in roots with high and low HK activity and possibly cause the observed alterations in growth in transgenic roots. The involvement of HK and futile cycles in the control of glucose-6P metabolism is discussed.
[Mh] Termos MeSH primário: Glucose/metabolismo
Hexoquinase/metabolismo
Plantas Geneticamente Modificadas
Solanum tuberosum
[Mh] Termos MeSH secundário: Metabolismo Energético
Hexosefosfatos/metabolismo
Fosforilação
Raízes de Plantas/enzimologia
Raízes de Plantas/metabolismo
Plantas Geneticamente Modificadas/enzimologia
Plantas Geneticamente Modificadas/metabolismo
Solanum tuberosum/enzimologia
Solanum tuberosum/metabolismo
Ciclização de Substratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hexosephosphates); EC 2.7.1.1 (Hexokinase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1309
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130206
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0053898



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