Готові списки джерел за темами / Phosphorylation oxidative

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Добірка наукової літератури з теми "Phosphorylation oxidative"

Автор: Grafiati
Опубліковано: 22 жовтня 2022

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Статті в журналах з теми "Phosphorylation oxidative"

1

Harper, Mary-Ellen, and Martin D. Brand. "Hyperthyroidism stimulates mitochondrial proton leak and ATP turnover in rat hepatocytes but does not change the overall kinetics of substrate oxidation reactions." Canadian Journal of Physiology and Pharmacology 72, no. 8 (August 1, 1994): 899–908. http://dx.doi.org/10.1139/y94-127.

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Thyroid hormones have well-known effects on oxidative phosphorylation, but there is little quantitative information on their important sites of action. We have used top-down elasticity analysis, an extension of metabolic control analysis, to identify the sites of action of thyroid hormones on oxidative phosphorylation in rat hepatocytes. We divided the oxidative phosphorylation system into three blocks of reactions: the substrate oxidation subsystem, the phosphorylating subsystem, and the mitochondrial proton leak subsystem and have identified those blocks of reactions whose kinetics are significantly changed by hyperthyroidism. Our results show significant effects on the kinetics of the proton leak and the phosphorylating subsystems. Quantitative analyses revealed that 43% of the increase in resting respiration rate in hyperthyroid hepatocytes compared with euthyroid hepatocytes was due to differences in the proton leak and 59% was due to differences in the activity of the phosphorylating subsystem. There were no significant effects on the substrate oxidation subsystem. Changes in nonmitochondrial oxygen consumption accounted for −2% of the change in respiration rate. Top-down control analysis revealed that the distribution of control over the rates of mitochondrial oxygen consumption, ATP synthesis and consumption, and proton leak and over mitochondrial membrane potential (Δψm) was similar in hepatocytes from hyperthyroid and littermate-paired euthyroid controls. The results of this study include the first complete top-down elasticity and control analyses of oxidative phosphorylation in hepatocytes from hyperthyroid rats.Key words: thyroid hormones, oxidative phosphorylation, mitochondria, proton leak, thermogenesis.
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2

Nath, Sunil, and John Villadsen. "Oxidative phosphorylation revisited." Biotechnology and Bioengineering 112, no. 3 (January 2, 2015): 429–37. http://dx.doi.org/10.1002/bit.25492.

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3

Hardin, Shane C., Clayton T. Larue, Man-Ho Oh, Vanita Jain, and Steven C. Huber. "Coupling oxidative signals to protein phosphorylation via methionine oxidation in Arabidopsis." Biochemical Journal 422, no. 2 (August 13, 2009): 305–12. http://dx.doi.org/10.1042/bj20090764.

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The mechanisms involved in sensing oxidative signalling molecules, such as H2O2, in plant and animal cells are not completely understood. In the present study, we tested the postulate that oxidation of Met (methionine) to MetSO (Met sulfoxide) can couple oxidative signals to changes in protein phosphorylation. We demonstrate that when a Met residue functions as a hydrophobic recognition element within a phosphorylation motif, its oxidation can strongly inhibit peptide phosphorylation in vitro. This is shown to occur with recombinant soybean CDPKs (calcium-dependent protein kinases) and human AMPK (AMP-dependent protein kinase). To determine whether this effect may occur in vivo, we monitored the phosphorylation status of Arabidopsis leaf NR (nitrate reductase) on Ser534 using modification-specific antibodies. NR was a candidate protein for this mechanism because Met538, located at the P+4 position, serves as a hydrophobic recognition element for phosphorylation of Ser534 and its oxidation substantially inhibits phosphorylation of Ser534in vitro. Two lines of evidence suggest that Met oxidation may inhibit phosphorylation of NR-Ser534in vivo. First, phosphorylation of NR at the Ser534 site was sensitive to exogenous H2O2 and secondly, phosphorylation in normal darkened leaves was increased by overexpression of the cytosolic MetSO-repair enzyme PMSRA3 (peptide MetSO reductase A3). These results are consistent with the notion that oxidation of surface-exposed Met residues in kinase substrate proteins, such as NR, can inhibit the phosphorylation of nearby sites and thereby couple oxidative signals to changes in protein phosphorylation.
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4

Shoffner, John. "Oxidative Phosphorylation Disease Diagnosis." Seminars in Neurology 19, no. 04 (1999): 341–51. http://dx.doi.org/10.1055/s-2008-1040849.

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5

Terada, H. "Uncouplers of oxidative phosphorylation." Environmental Health Perspectives 87 (July 1990): 213–18. http://dx.doi.org/10.1289/ehp.9087213.

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6

SHOFFNER, JOHN M. "Oxidative Phosphorylation Disease Diagnosis." Annals of the New York Academy of Sciences 893, no. 1 OXIDATIVE/ENE (November 1999): 42. http://dx.doi.org/10.1111/j.1749-6632.1999.tb07817.x.

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7

Lesnefsky, Edward J., and Charles L. Hoppel. "Oxidative phosphorylation and aging." Ageing Research Reviews 5, no. 4 (November 2006): 402–33. http://dx.doi.org/10.1016/j.arr.2006.04.001.

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8

Schatz, Gottfried. "Mitochondria: beyond oxidative phosphorylation." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1271, no. 1 (May 1995): 123–26. http://dx.doi.org/10.1016/0925-4439(95)00018-y.

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9

Hu, Yuanyu, Xueying Wang, Li Zeng, De-Yu Cai, Kanaga Sabapathy, Stephen P. Goff, Eduardo J. Firpo, and Baojie Li. "ERK Phosphorylates p66shcA on Ser36 and Subsequently Regulates p27kip1 Expression via the Akt-FOXO3a Pathway: Implication of p27kip1 in Cell Response to Oxidative Stress." Molecular Biology of the Cell 16, no. 8 (August 2005): 3705–18. http://dx.doi.org/10.1091/mbc.e05-04-0301.

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Mice deficient for p66shcA represent an animal model to link oxidative stress and aging. p66shcA is implicated in oxidative stress response and mitogenic signaling. Phosphorylation of p66shcA on Ser36 is critical for its function in oxidative stress response. Here we report the identification of ERK as the kinase phosphorylating p66shcA on Ser36. Activation of ERKs was necessary and sufficient for Ser36 phosphorylation. p66shcA interacted with ERK and was demonstrated to be a substrate for ERK, with Ser36 being the major phosphorylation site. Furthermore, in response to H2O2, inhibition of ERK activation repressed p66shcA-dependent phosphorylation of FOXO3a and the down-regulation of its target gene p27kip1. Down-regulation of p27 might promote cell survival, as p27 played a proapoptotic role in oxidative stress response. As a feedback regulation, Ser36 phosphorylated p66shcA attenuated H2O2-induced ERK activation, whereas p52/46shcA facilitated ERK activation, which required tyrosine phosphorylation of CH1 domain. p66shcA formed a complex with p52/46ShcA, which may provide a platform for efficient signal propagation. Taken together, the data suggest there exists an interplay between ERK and ShcA proteins, which modulates the expression of p27 and cell response to oxidative stress.
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10

Umida, Yusupova, Mamatova Zulaykho, Dzhabbarova Gulchehra, Tukhtaeva Feruza, and Almatov Karim. "Influence Of Galangin On Respiration And Oxidative Phosphorylation Of Rat Liver Mitochondria." American Journal of Agriculture and Biomedical Engineering 02, no. 06 (June 23, 2020): 14–23. http://dx.doi.org/10.37547/tajabe/volume02issue06-02.

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Дисертації з теми "Phosphorylation oxidative"

1

Carr, M. D. "NMR studies of oxidative phosphorylation." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382584.

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2

Eijsden, Rudy Gerardus Elisabeth van. "Microarray analysis of oxidative phosphorylation disorders." [Maastricht] : Maastricht : Maastricht University ; University Library, Universiteit Maastricht [host], 2008. http://arno.unimaas.nl/show.cgi?fid=10708.

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3

Heiske, Margit. "Modeling the respiratory chain and the oxidative phosphorylation." Thesis, Bordeaux 2, 2012. http://www.theses.fr/2012BOR21965/document.

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Mitochondria are cell organelles which play an essential role in the cell energy supply providing the universal high energetic molecule ATP which is used in numerous energy consuming processes. The core of the ATP production, oxidative phosphorylation (OXPHOS) consists of four enzyme complexes (respiratory chain) which establish, driven by redox reactions, a proton gradient over the inner mitochondrial membrane. The ATP-synthase uses this electrochemical gradient to phosphorylate ADP to ATP. Dysfunctioning of an OXPHOS complex can have severe consequences for the energy metabolism and cause rare but incurable dysfunctions in particular tissues with a high energy demand such as brain, heart, kidney and skeleton muscle. Moreover mitochondria are linked to widespread diseases like diabetes, cancer, Alzheimer and Parkinson. Further, reactive oxygen species which are a by-product of the respiratory chain, are supposed to play a crucial role in aging. The aim of this work is to provide a realistic model of OXPHOS which shall help understanding and predicting the interactions within the OXPHOS and how a local defect (enzyme deficiency or modification) is expressed globally in mitochondrial oxygen consumption and ATP synthesis. Therefore we chose a bottom-up approach. In a first step different types of rate equations were analyzed regarding their ability to describe the steady state kinetics of the isolated respiratory chain complexes in the absence of the proton gradient. Here Michaelis-Menten like rate equations were revealed to be appropriate for describing their behavior over a wide range of substrate and product concentrations. For the validation of the equations and the parameter estimation we have performed kinetic measurements on bovine heart submitochondrial particles. The next step consisted in the incorporation of the proton gradient into the rate equations, distributing its influence among the kinetic parameters such that reasonable rates were obtained in the range of physiological electrochemical potential differences. In the third step, these new individual kinetic rate expressions for the OXPHOS complexes were integrated in a global model of oxidative phosphorylation. The new model could fit interrelated data of oxygen consumption, the transmembrane potential and the redox state of electron carriers. Furthermore, flux inhibitor titration curves can be well reproduced, which validates its global responses to local effects. This model may be of great help to understand the increasingly recognized role of mitochondria in many cell processes and diseases as illustrated by some simulations proposed in this work
Les mitochondries sont l’usine à énergie de la cellule. Elles synthétisent l’ATP à partir d’une succession de réactions d’oxydo-réduction catalysées par quatre complexes respiratoires qui forment la chaîne respiratoire. Avec la machinerie de synthèse d’ATP l’ensemble constitue les oxydations phosphorylantes (OXPHOS). Le but de ce travail est de bâtir un modèle des OXPHOS basé sur des équations de vitesse simples mais thermodynamiquement correctes, représentant l’activité des complexes de la chaîne respiratoire (équations de type Michaelis- Menten). Les paramètres cinétiques de ces équations sont identifiés en utilisant les cinétiques expérimentales de ces complexes respiratoires réalisées en absence de gradient de proton. La phase la plus délicate de ce travail a résidé dans l’introduction du gradient de protons dans ces équations. Nous avons trouvé que la meilleure manière était de distribuer l’effet du gradient de proton sous forme d’une loi exponentielle sur l’ensemble des paramètres, Vmax et Km pour les substrats et les produits. De cette manière, j’ai montré qu’il était possible de représenter les variations d’oxygène, de ΔΨ et de ΔpH trouvés dans la littérature. De plus, contrairement aux autres modèles, il fut possible de simuler les courbes de seuil observées expérimentalement lors de la titration du flux de respiration par l’inhibiteur d’un complexe respiratoire donné.Ce modèle pourra présenter un très grand intérêt pour comprendre le rôle de mieux en mieux reconnu des mitochondries dans de nombreux processus cellulaires, tels que la production d’espèces réactives de l’oxygène, le vieillissement, le diabète, le cancer, les pathologies mitochondriales etc. comme l’illustrent un certain nombre de prédictions présentées dans ce travail
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4

Heiske, Margit. "Modeling the respiratory chain and the oxidative phosphorylation." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2013. http://dx.doi.org/10.18452/16720.

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Die oxidative Phosphorylierung (OXPHOS) spielt eine zentrale Rolle im Energiestoffwechsel der Zelle. Sie besteht aus der Atmungskette, deren vier Enzymkomplexe einen Protonengradienten über die innere mitochondriale Membran aufbauen, und der ATP-Synthase, die diesen Gradienten zur Phosphorylierung von ADP zu ATP, der zelluläre Energieeinheit, nutzt. In der vorliegenden Arbeit wurde ein thermodynamisch konformes OXPHOS Modell erstellt, welches auf Differentialgleichungen basiert. Dazu wurden Gleichungen entwickelt, welche die Kinetiken jedes OXPHOS-Komplexes über weite Bereiche von Substrat- und Produktkonzentrationen sowie unterschiedlichster Werte des elektrochemischen Gradientens wiedergeben. Zunächst wurden für jeden Komplex der Atmungskette kinetische Messungen in Abwesenheit des Protonengradientens durchgeführt. Für deren Beschreibung erwiesen sich Gleichungen vom Typ Michaelis-Menten als adäquat; hierbei wurden verschiedene Gleichungstypen verglichen. Anschließend wurde der Einfluss des Protonengradientens auf die kinetischen Parameter so modelliert, dass physiologisch sinnvolle Raten in dessen Abhängigkeit erzielt werden konnten. Diese neuen Ratengleichungen wurden schließlich in ein OXPHOS Modell integriert, mit dem sich experimentelle Daten von Sauerstoffverbrauch, elektrischem Potential und pH-Werten sehr gut beschreiben ließen. Weiter konnten Inhibitor-Titrationskurven reproduziert werden, welche den Sauerstoffverbrauch in Abhängigkeit der relativen Hemmung eines OXPHOS-Komplexes darstellen. Dies zeigt, dass lokale Effekte auf globaler Ebene korrekt wiedergeben werden können. Das hier erarbeitete Modell ist eine solide Basis, um die Rolle der OXPHOS und generell von Mitochondrien eingehend zu untersuchen. Diese werden mit zahlreichen zellulären Vorgängen in Verbindung gebracht: unter anderem mit Diabetes, Krebs und Mitochodriopathien, sowie der Bildung von Sauerstoffradikalen, die im Zusammenhang mit Alterungsprozessen stehen.
Oxidative phosphorylation (OXPHOS) plays a central role in the cellular energy metabolism. It comprises the respiratory chain, consisting of four enzyme complexes that establish a proton gradient over the inner mitochondrial membrane, and the ATP-synthase that uses this electrochemical gradient to phosphorylate ADP to ATP, the cellular energy unit. In this work a thermodynamically consistent OXPHOS model was built based on a set of differential equations. Therefore rate equations were developed that describe the kinetics of each OXPHOS complex over a wide concentration range of substrates and products as well for various values of the electrochemical gradient. In a first step, kinetic measurements on bovine heart submitochondrial particles have been performed in the absence of the proton gradient. An appropriate data description was achieved with Michaelis-Menten like equations; here several types of equations have been compared. The next step consisted in incorporating the proton gradient into the rate equations. This was realized by distributing its influence among the kinetic parameters such that reasonable catalytic rates were obtained under physiological conditions. Finally, these new individual kinetic rate expressions for the OXPHOS complexes were integrated in a global model of oxidative phosphorylation. This new model could fit interrelated data of oxygen consumption, the transmembrane potential and the redox state of electron carriers. Furthermore, it could well reproduce flux inhibitor titration curves, which validates its global responses to local perturbations. This model is a solid basis for analyzing the role of OXPHOS and mitochondria in detail. They have been linked to various cellular processes like diabetes, cancer, mitochondrial disorders, but also to the production of reactive oxygen species, which are supposed to be involved in aging.
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5

Luca, Corneliu Constantin. "MTERFD3 is a Mitochondrial Protein that Modulates Oxidative Phosphorylation." Scholarly Repository, 2008. http://scholarlyrepository.miami.edu/oa_dissertations/132.

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Mitochondrial function is critical for the survival of eukaryotes. Hence, mitochondrial dysfunctions are involved in numerous human diseases. An essential process for a normal mitochondrial function is mitochondrial gene expression which is tightly regulated in response to various physiological changes. The accurate control of mitochondrial gene expression is essential in order to provide the appropriate oxidative phosphorylation capacity for diverse metabolic demands. Recent findings in the basic mitochondrial replication and transcription regulation helped advance our understanding of organelle function and basic pathogenetic mechanisms of mitochondrial DNA mutations associated with oxidative phosphorylation defects. Mitochondrial transcription is regulated by the mitochondrial transcription termination factor (mTERF) both at the initiation and termination levels. A protein family containing highly conserved mTERF motifs has been identified recently and its members named generically as "terfins." In this work, one of these factors, mTERFD3, has been characterized in vitro and in vivo. The mTERFD3 protein is highly conserved throughout evolution. It is a mitochondrial protein localized to the matrix and is abundantly expressed in high energy demand tissues. We found that it contains 4 putative leucine zippers and is able to form dimers in vitro. We showed that mTERFD3 binds mtDNA at the transcription initiation site in the mtDNA regulatory region. These findings suggest that mTERFD3 may be involved in regulating mitochondrial gene expression at the transcriptional initiation level. In order to study the functional significance of mTERFD3 in vivo we developed a mouse deficient in mTERFD3 using a gene trapping strategy. The KO mice had a normal lifespan but showed decreased weight gain and decreased fat content in females. Fibroblasts isolated from KO mice displayed decreased growth rate when compared with WT in respiratory media, and had decreased complex IV activity. Consistent with the above findings, we found that muscle, one of the tissues with high energy demands, showed abnormal mitochondrial function, displaying features characteristic of mitochondrial myopathy such as decreased muscle strength and endurance. Muscle mitochondria of the KO mice showed a significant decrease in the complex II +III and complex IV activity. The decrease in OXPHOS complexes activity was associated with increased citrate synthase activity, suggesting mitochondrial proliferation, a feature typical for mitochondrial disorders. Another important finding was a decrease in the muscle mitochondrial transcripts in the KO animals associated with decreased steady state levels of OXPHOS subunits. Together these data suggest that mTERFD3 is a mitochondrial protein involved in the regulation of mtDNA transcription. mTERFD3 KO is not embryonic lethal suggesting that it is involved in the fine tuning of mitochondrial transcription. We conclude that mTERFD3 is a mitochondrial protein that modulates oxidative phosphorylation function, probably by directed interactions with the mtDNA regulatory region. This work shows the importance of mTERFD3, an mTERF family member, in the mitochondrial gene expression regulation.
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6

Padovan, Anna Caterina. "The control of oxidative phosphorylation in isolated plant mitochondria /." Title page, table of contents and summary only, 1986. http://web4.library.adelaide.edu.au/theses/09SB/09sbp124.pdf.

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7

Schroeder, James Lee. "Acute and chronic regulation of oxidative phosphorylation in muscle." Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.540256.

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8

Kavanagh, Norita Irene. "A quantitative analysis of the effect of calcium on oxidative phosphorylation." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624736.

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9

Žūkienė, Rasa. "Investigation of the effect of hyperthermic treatment on mitochondrial oxidative phosphorylation system." Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2008. http://vddb.library.lt/obj/LT-eLABa-0001:E.02~2008~D_20081120_151452-51127.

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The elucidation of the molecular mechanism of the cell response to moderate heating is of importance for understanding the events that occur in the cell upon use of heating for therapeutic purpose or during illnesses that are associated with fever. The aim of this work was to investigate and to compare the effects of mild (fever) and severe hyperthermia on functional properties of oxidative phosphorylation system in normal tissue mitochondria. Modular kinetic analysis for the first time was applied to evaluate effects of hyperthermia on oxidative phosphorylation in rat heart and liver mitochondria. We demonstrated that changes in mitochondrial functions induced by mild hyperthermia (42 ºC) are reversible but more severe hyperthermia (45 ºC) causes partially irreversible uncoupling and inhibition of mitochondrial respiration in state 3, hyperthermia remarkably (3.6-2.1 fold) activates ROS generation in heart mitochondria and that maximal increase in rate of H2O2 production and lipid peroxidation is observed in the fever temperature range. We show that the response of liver mitochondria and hepatocytes to hyperthermia is to certain extent dependent on gender and temperature. Specific differences of male rat liver and heart mitochondrial components phase transitions have been revealed by DSC analysis.
Ląstelių atsako į nuosaikią hipertermiją molekulinio mechanizmo išaiškinimas yra labai svarbus norint suprasti procesus, kurie vyksta ląstelėse jas kaitinant gydymo tikslais ar organizmui karščiuojant. Šio darbo tikslas buvo nustatyti ir palyginti švelnios (karščiavimo) ir šiurkščios hipertermijos poveikį oksidacinės fosforilinimo sistemos funkcijoms normalių audinių mitochondrijose. Pirmą kartą panaudojome modulių kinetinę analizę hipertermijos poveikiui širdies ir kepenų mitochondrijų oksidacinio fosforilinimo sistemai tirti. Mes nustatėme, kad švelnios hipertermijos (42 ºC) poveikis širdies mitochondrijų funkcijoms yra grįžtamas, bet šiurkštesnė hipertermija (45 ºC) sukelia dalinai negrįžtamą kvėpavimo ir fosforilinimo atskyrimą bei mitochondrijų kvėpavimo greičio trečioje metabolinėje būsenoje slopinimą. Hipertermija didino ROS gamybos greitį ir lipidų peroksidaciją, kurie buvo didžiausi karščiavimo temperatūroje. Nustatėme, kad kepenų mitochondrijų ir hepatocitų atsakas į hipertermiją priklauso nuo žiurkės lyties ir temperatūros. Atlikome palyginamąjį širdies ir kepenų mitochondrijų sandų fazinių virsmų analizę diferencine skenuojamaja kalorimetrija ir nustatėme būdingus skirtumus.
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Liu, Quan. "PHOSPHORYLATION AND SEQUENCE DEPENDENCY OF NEUROFILAMENT PROTEIN OXIDATIVE MODIFICATION IN ALZHEIMER DISEASE." Connect to text online, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1102024839.

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Книги з теми "Phosphorylation oxidative"

1

Kadenbach, Bernhard, ed. Mitochondrial Oxidative Phosphorylation. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3573-0.

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2

Smeitink, Jan A. M., Rob C. A. Sengers, and J. M. Frans Trijbels. Oxidative Phosphorylation in Health and Disease. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/b138432.

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3

Saraste, Matti. Oxidative phosphorylation at the 'fin de siècle'. Washington, D.C: American Association for the Advancement of Science, 1999.

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4

Teijeiro, Isabel. Effects of oxidative phosphorylation inhibitors on the growth and viability of Saccharmomyces cerevisiae. Sudbury, Ont: Laurentian University, 1997.

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5

Winegarden, Neil Anthony. The effect of inhibitors of oxidative phosphorylation on the dorsophila heat shock response. Ottawa: National Library of Canada, 1997.

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6

Oxidative Phosphorylation. Landes Bioscience, 2003.

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7

Biological Energy Conservation: Oxidative Phosphorylation. Springer, 2012.

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8

M, Smeitink Jan A., Sengers Rob C. A, and Trijbels J. M. Frans, eds. Oxidative phosphorylation in health and disease. Georgetown, Tex., U.S.A: Landes Bioscience/Eurekah.com, 2004.

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9

Smeitink, Jan A. M. Oxidative Phosphorylation in Health and Disease. Springer, 2004.

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10

Oxidative phosphorylation in health and disease. Georgetown, TX: Landes Bioscience/Eurekah.com, 2005.

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Частини книг з теми "Phosphorylation oxidative"

1

Gooch, Jan W. "Oxidative Phosphorylation." In Encyclopedic Dictionary of Polymers, 912. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14414.

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Baak, Marleen A., Bernard Gutin, Kim A. Krawczewski Carhuatanta, Stephen C. Woods, Heinz W. Harbach, Megan M. Wenner, Nina S. Stachenfeld, et al. "Oxidative Phosphorylation." In Encyclopedia of Exercise Medicine in Health and Disease, 679. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2816.

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3

Ochs, Raymond S. "Oxidative Phosphorylation." In Biochemistry, 235–64. 2nd ed. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9781003029649-11.

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Burgot, Jean-Louis. "Oxidative Phosphorylation— Photosynthesis." In Thermodynamics in Bioenergetics, 255–65. Boca Raton, FL : CRC Press, 2019. | “A science publishers book.”: CRC Press, 2019. http://dx.doi.org/10.1201/9781351034227-36.

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Shoffner, John M., and Douglas C. Wallace. "Oxidative Phosphorylation Diseases." In Advances in Human Genetics, 267–330. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4757-9065-8_5.

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Oette, Mark, Marvin J. Stone, Hendrik P. N. Scholl, Peter Charbel Issa, Monika Fleckenstein, Steffen Schmitz-Valckenberg, Frank G. Holz, et al. "Mitochondrial Oxidative Phosphorylation Disorders." In Encyclopedia of Molecular Mechanisms of Disease, 1331–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6255.

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Okey, Robert W., and H. D. Stensel. "Uncouplers of Oxidative Phosphorylation." In Emerging Technologies in Hazardous Waste Management V, 284–309. Washington, DC: American Chemical Society, 1995. http://dx.doi.org/10.1021/bk-1995-0607.ch022.

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Rahman, Shamima, and Johannes A. Mayr. "Disorders of Oxidative Phosphorylation." In Inborn Metabolic Diseases, 223–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-49771-5_14.

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de Laat, Paul, Richard Rodenburg, and Jan Smeitink. "Mitochondrial Oxidative Phosphorylation Disorders." In Physician's Guide to the Diagnosis, Treatment, and Follow-Up of Inherited Metabolic Diseases, 337–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-40337-8_22.

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Rahman, Shamima, and Johannes A. Mayr. "Disorders of Oxidative Phosphorylation." In Inborn Metabolic Diseases, 247–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 2022. http://dx.doi.org/10.1007/978-3-662-63123-2_10.

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Тези доповідей конференцій з теми "Phosphorylation oxidative"

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"Subcompartmented oxphosomic model of the mitochondrial oxidative phosphorylation system." In Plant Genetics, Genomics, Bioinformatics, and Biotechnology. Novosibirsk ICG SB RAS 2021, 2021. http://dx.doi.org/10.18699/plantgen2021-210.

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Moschos, Stergios J., Michelle Barbi de Moura, Shelley Fayewicz, Nicholas Bateman, Mai Sun, Stefan Duensing, Yan Yin, et al. "Abstract B144: Elesclomol, an inducer of oxidative stress, targets oxidative phosphorylation (oxphos) in melanoma cells." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-b144.

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ANTONENKO, YURI N. "NEW UNCOUPLERS OF OXIDATIVE PHOSPHORYLATION: BAM15, PYRROLOMYCIN AND USNIC ACID." In HOMO SAPIENS LIBERATUS. TORUS PRESS, 2020. http://dx.doi.org/10.30826/homosapiens-2020-13.

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Adeshakin, Funmilayo Oladunni, Guizhong Zhang, Adeleye O. Adeshakin, and Xiaochun Wan. "Abstract 2869: Blockade of oxidative phosphorylation by metformin promotes anoikis." 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.am2021-2869.

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Janiszewska, Michalina, Mario-Luca Suva, Nicolo Riggi, and Ivan Stamenkovic. "Abstract 1137: Imp2 controls oxidative phosphorylation in glioblastoma cancer stem cells." 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.am2012-1137.

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Jewell, Brittany E., An Xu, Ruoji Zhou, Dandan Zhu, Linchao Lu, Ruying Zhao, Lisa L. Wang, and Dung-Fang Lee. "Abstract B36: A novel model of osteosarcomagenesis reveals dysregulation of oxidative phosphorylation." In Abstracts: AACR Special Conference on the Advances in Pediatric Cancer Research; September 17-20, 2019; Montreal, QC, Canada. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.pedca19-b36.

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Koromilas, Antonis E., Rajesh Kamindla, Andreas I. Papadakis, Urszula Kazimierczak, Philippos Peidis, Shuo Wang, Clara Tenkerian, et al. "Abstract C51: eIF2alpha phosphorylation determines cell susceptibility to oxidative stress via Akt activation." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-c51.

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Geng, Guannan, Huijing Wang, and Shuang Ye. "231 tRNA derived fragments(tRFs) regulate oxidative phosphorylation to participate in SLE pathogenesis." In 13th International Congress on Systemic Lupus Erythematosus (LUPUS 2019), San Francisco, California, USA, April 5–8, 2019, Abstract Presentations. Lupus Foundation of America, 2019. http://dx.doi.org/10.1136/lupus-2019-lsm.231.

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Meric-Bernstam, Funda, Kurt Evans, Xiaofeng Zheng, Xiaoping Su, Erkan Yuca, Stephen Scott, Argun Akcakanat, et al. "Abstract 4970: Oxidative phosphorylation as a target in triple negative breast cancer therapy." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4970.

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Jia, Dongya, Linglin Yu, Mingyang Lu, Eshel Ben-Jacob, Jianpeng Ma, Herbert Levine, Benny A. Kaipparettu, and Jose Onuchic. "Abstract 5568: Towards decoding the interplay between glycolysis and oxidative phosphorylation in cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5568.

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Звіти організацій з теми "Phosphorylation oxidative"

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Elmann, Anat, Orly Lazarov, Joel Kashman, and Rivka Ofir. therapeutic potential of a desert plant and its active compounds for Alzheimer's Disease. United States Department of Agriculture, March 2015. http://dx.doi.org/10.32747/2015.7597913.bard.

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Анотація:
We chose to focus our investigations on the effect of the active forms, TTF and AcA, rather than the whole (crude) extract. 1. To establish cultivation program designed to develop lead cultivar/s (which will be selected from the different Af accessions) with the highest yield of the active compounds TTF and/or achillolide A (AcA). These cultivar/s will be the source for the purification of large amounts of the active compounds when needed in the future for functional foods/drug development. This task was completed. 2. To determine the effect of the Af extract, TTF and AcA on neuronal vulnerability to oxidative stress in cultured neurons expressing FAD-linked mutants.Compounds were tested in N2a neuroblastoma cell line. In addition, we have tested the effects of TTF and AcA on signaling events promoted by H₂O₂ in astrocytes and by β-amyloid in neuronal N2a cells. 3. To determine the effect of the Af extract, TTF and AcA on neuropathology (amyloidosis and tau phosphorylation) in cultured neurons expressing FAD-linked mutants. 4. To determine the effect of A¦ extract, AcA and TTF on FAD-linked neuropathology (amyloidosis, tau phosphorylation and inflammation) in transgenic mice. 5. To examine whether A¦ extract, TTF and AcA can reverse behavioral deficits in APPswe/PS1DE9 mice, and affect learning and memory and cognitive performance in these FAD-linked transgenic mice. Background to the topic.Neuroinflammation, oxidative stress, glutamate toxicity and amyloid beta (Ab) toxicity are involved in the pathogenesis of Alzheimer's diseases. We have previously purified from Achilleafragrantissimatwo active compounds: a protective flavonoid named 3,5,4’-trihydroxy-6,7,3’-trimethoxyflavone (TTF, Fl-72/2) and an anti-inflammatory sesquiterpenelactone named achillolide A (AcA). Major conclusions, solutions, achievements. In this study we could show that TTF and AcA protected cultured astrocytes from H₂O₂ –induced cell death via interference with cell signaling events. TTF inhibited SAPK/JNK, ERK1/2, MEK1 and CREBphosphorylation, while AcA inhibited only ERK1/2 and MEK1 phosphorylation. In addition to its protective activities, TTF had also anti-inflammatory activities, and inhibited the LPS-elicited secretion of the proinflammatorycytokinesInterleukin 6 (IL-6) and IL-1b from cultured microglial cells. Moreover, TTF and AcA protected neuronal cells from glutamate and Abcytotoxicity by reducing the glutamate and amyloid beta induced levels of intracellular reactive oxygen species (ROS) and via interference with cell signaling events induced by Ab. These compounds also reduced amyloid precursor protein net processing in vitro and in vivo in a mouse model for Alzheimer’s disease and improvedperformance in the novel object recognition learning and memory task. Conclusion: TTF and AcA are potential candidates to be developed as drugs or food additives to prevent, postpone or ameliorate Alzheimer’s disease. Implications, both scientific and agricultural.The synthesis ofAcA and TTF is very complicated. Thus, the plant itself will be the source for the isolation of these compounds or their precursors for synthesis. Therefore, Achilleafragrantissima could be developed into a new crop with industrial potential for the Arava-Negev area in Israel, and will generate more working places in this region.
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Or, Etti, David Galbraith, and Anne Fennell. Exploring mechanisms involved in grape bud dormancy: Large-scale analysis of expression reprogramming following controlled dormancy induction and dormancy release. United States Department of Agriculture, December 2002. http://dx.doi.org/10.32747/2002.7587232.bard.

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Анотація:
The timing of dormancy induction and release is very important to the economic production of table grape. Advances in manipulation of dormancy induction and dormancy release are dependent on the establishment of a comprehensive understanding of biological mechanisms involved in bud dormancy. To gain insight into these mechanisms we initiated the research that had two main objectives: A. Analyzing the expression profiles of large subsets of genes, following controlled dormancy induction and dormancy release, and assessing the role of known metabolic pathways, known regulatory genes and novel sequences involved in these processes B. Comparing expression profiles following the perception of various artificial as well as natural signals known to induce dormancy release, and searching for gene showing similar expression patterns, as candidates for further study of pathways having potential to play a central role in dormancy release. We first created targeted EST collections from V. vinifera and V. riparia mature buds. Clones were randomly selected from cDNA libraries prepared following controlled dormancy release and controlled dormancy induction and from respective controls. The entire collection (7920 vinifera and 1194 riparia clones) was sequenced and subjected to bioinformatics analysis, including clustering, annotations and GO classifications. PCR products from the entire collection were used for printing of cDNA microarrays. Bud tissue in general, and the dormant bud in particular, are under-represented within the grape EST database. Accordingly, 59% of the our vinifera EST collection, composed of 5516 unigenes, are not included within the current Vitis TIGR collection and about 22% of these transcripts bear no resemblance to any known plant transcript, corroborating the current need for our targeted EST collection and the bud specific cDNA array. Analysis of the V. riparia sequences yielded 814 unigenes, of which 140 are unique (keilin et al., manuscript, Appendix B). Results from computational expression profiling of the vinifera collection suggest that oxidative stress, calcium signaling, intracellular vesicle trafficking and anaerobic mode of carbohydrate metabolism play a role in the regulation and execution of grape-bud dormancy release. A comprehensive analysis confirmed the induction of transcription from several calcium–signaling related genes following HC treatment, and detected an inhibiting effect of calcium channel blocker and calcium chelator on HC-induced and chilling-induced bud break. It also detected the existence of HC-induced and calcium dependent protein phosphorylation activity. These data suggest, for the first time, that calcium signaling is involved in the mechanism of dormancy release (Pang et al., in preparation). We compared the effects of heat shock (HS) to those detected in buds following HC application and found that HS lead to earlier and higher bud break. We also demonstrated similar temporary reduction in catalase expression and temporary induction of ascorbate peroxidase, glutathione reductase, thioredoxin and glutathione S transferase expression following both treatments. These findings further support the assumption that temporary oxidative stress is part of the mechanism leading to bud break. The temporary induction of sucrose syntase, pyruvate decarboxylase and alcohol dehydrogenase indicate that temporary respiratory stress is developed and suggest that mitochondrial function may be of central importance for that mechanism. These finding, suggesting triggering of identical mechanisms by HS and HC, justified the comparison of expression profiles of HC and HS treated buds, as a tool for the identification of pathways with a central role in dormancy release (Halaly et al., in preparation). RNA samples from buds treated with HS, HC and water were hybridized with the cDNA arrays in an interconnected loop design. Differentially expressed genes from the were selected using R-language package from Bioconductor project called LIMMA and clones showing a significant change following both HS and HC treatments, compared to control, were selected for further analysis. A total of 1541 clones show significant induction, of which 37% have no hit or unknown function and the rest represent 661 genes with identified function. Similarly, out of 1452 clones showing significant reduction, only 53% of the clones have identified function and they represent 573 genes. The 661 induced genes are involved in 445 different molecular functions. About 90% of those functions were classified to 20 categories based on careful survey of the literature. Among other things, it appears that carbohydrate metabolism and mitochondrial function may be of central importance in the mechanism of dormancy release and studies in this direction are ongoing. Analysis of the reduced function is ongoing (Appendix A). A second set of hybridizations was carried out with RNA samples from buds exposed to short photoperiod, leading to induction of bud dormancy, and long photoperiod treatment, as control. Analysis indicated that 42 genes were significant difference between LD and SD and 11 of these were unique.
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