Gotowe bibliografie tematyczne / Nicotinamide adenine dinucleotide

Gotowa bibliografia na temat „Nicotinamide adenine dinucleotide”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 20 lutego 2023

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Artykuły w czasopismach na temat "Nicotinamide adenine dinucleotide"

Alberty, R. A. "Thermodynamics of Reactions of Nicotinamide Adenine Dinucleotide and Nicotinamide Adenine Dinucleotide Phosphate". Archives of Biochemistry and Biophysics 307, nr 1 (listopad 1993): 8–14. http://dx.doi.org/10.1006/abbi.1993.1552.

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Micheli, Vanna, H. Anne Simmonds i Carlo Ricci. "Regulation of nicotinamide–adenine dinucleotide synthesis in erythrocytes of patients with hypoxanthine–guanine phosphoribosyltransferase deficiency and a patient with phosphoribosylpyrophosphate synthetase superactivity". Clinical Science 78, nr 2 (1.02.1990): 239–45. http://dx.doi.org/10.1042/cs0780239.

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1. The synthesis of nicotinamide–adenine dinucleotide from nicotinamide and nicotinic acid was compared over different time scales at both physiological (0.7 μmol/l) and high (0.2–3 mmol/l) substrate concentrations in erythrocytes from three patients with hypoxanthine–guanine phosphoribosyltransferase (hypoxanthine phosphoribosyltransferase, EC 2.4.2.8) deficiency (including one Lesch–Nyhan patient) and from one patient with phosphoribosylpyrophosphate synthetase superactivity. The above disorders are associated with grossly altered erythrocyte nicotinamide-adenine dinucleotide levels. 2. At the physiological substrate concentration and incubation times up to 2 h, nicotinamide proved the most efficient nicotinamide–adenine dinucleotide precursor for erythrocytes from both patients and control subjects. The conversion of nicotinamide to its mononucleotide, but not further metabolism, was impaired in phosphoribosylpyrophosphate synthetase-mutant cells. The Lesch–Nyhan and phosphoribosylpyrophosphate synthetase-mutant cells were unusual in that both showed no further stimulation of nucleotide synthesis at 18 mmol/l Pi compared with 1 mmol/l. 3. At the high substrate concentrations, using 18 mmol/l Pi, nicotinamide was a poor precursor in all instances. Using nicotinic acid, nucleotide formation was 30-fold that from nicotinamide, reaching its maximum at 0.2 mmol/l. Conversion of nicotinic acid to nicotinamide–adenine dinucleotide in the phosphoribosylpyrophosphate synthetase-mutant cells was again grossly impaired. 4. There was no evidence for increased nicotinamide–adenine dinucleotide breakdown in the phosphoribosylpyrophosphate synthetase-mutant cells under any of the above conditions. 5. These results suggest that the differing nicotinamide–adenine dinucleotide levels in the two disorders cannot be related directly to the altered phosphoribosylpyrophosphate levels. The problem appears to be one of decreased synthesis in the phosphoribosylpyrophosphate synthetase-mutant cells, whereas the synthetic capacity in intact hypoxanthine–guanine phosphoribosyltransferase-deficient cells is neither enhanced nor inhibited by the raised nicotinamide–adenine dinucleotide levels.

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Pankiewicz, K., L. Chen, R. Petrelli, K. Felczak, G. Gao, L. Bonnac, J. Yu i E. Bennett. "Nicotinamide Adenine Dinucleotide Based Therapeutics". Current Medicinal Chemistry 15, nr 7 (1.03.2008): 650–70. http://dx.doi.org/10.2174/092986708783885282.

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Frederick, David W., Sophie Trefely, Alexia Buas, Jason Goodspeed, Jay Singh, Clementina Mesaros, Joseph A. Baur i Nathaniel W. Snyder. "Stable isotope labeling by essential nutrients in cell culture (SILEC) for accurate measurement of nicotinamide adenine dinucleotide metabolism". Analyst 142, nr 23 (2017): 4431–37. http://dx.doi.org/10.1039/c7an01378g.

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Nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP) are conserved metabolic cofactors that mediate reduction-oxidation (redox) reactions throughout all domains of life.

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Kova´rˇ, J., J. Tura´nek, C. Hlava´cˇ, V. Vala i V. Kahle. "Liquid chromatographic separations of dimers of nicotinamide adenine dinucleotide and nicotinamide adenine dinucleotide phosphate". Journal of Chromatography A 319 (styczeń 1985): 341–49. http://dx.doi.org/10.1016/s0021-9673(01)90570-9.

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Lee, H. J., i G. G. Chang. "Interactions of nicotinamide-adenine dinucleotide phosphate analogues and fragments with pigeon liver malic enzyme. Synergistic effect between the nicotinamide and adenine moieties". Biochemical Journal 245, nr 2 (15.07.1987): 407–14. http://dx.doi.org/10.1042/bj2450407.

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The structural requirements of the NADP+ molecule as a coenzyme in the oxidative decarboxylation reaction catalysed by pigeon liver malic enzyme were studied by kinetic and fluorimetric analyses with various NADP+ analogues and fragments. The substrate L-malate had little effect on the nucleotide binding. Etheno-NADP+, 3-acetylpyridine-adenine dinucleotide phosphate, and nicotinamide-hypoxanthine dinucleotide phosphate act as alternative coenzymes for the enzyme. Their kinetic parameters were similar to that of NADP+. Thionicotinamide-adenine dinucleotide phosphate, 3-aminopyridine-adenine dinucleotide phosphate, 5′-adenylyl imidodiphosphate, nicotinamide-adenine dinucleotide 3′-phosphate and NAD+ act as inhibitors for the enzyme. The first two were competitive with respect to NADP+ and non-competitive with respect to L-malate; the other inhibitors were non-competitive with NADP+. All NADP+ fragments were inhibitory to the enzyme, with a wide range of affinity, depending on the presence or absence of a 2′-phosphate group. Compounds with this group bind to the enzyme 2-3 orders of magnitude more tightly than those without this group. Only compounds with this group were competitive inhibitors with respect to NADP+. We conclude that the 2′-phosphate group is crucial for the nucleotide binding of this enzyme, whereas the carboxyamide carbonyl group of the nicotinamide moiety is important for the coenzyme activity. There is a strong synergistic effect between the binding of the nicotinamide and adenosine moieties of the nucleotide molecule.

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Merk, Virginia, Eugen Speiser, Wolfgang Werncke, Norbert Esser i Janina Kneipp. "pH-Dependent Flavin Adenine Dinucleotide and Nicotinamide Adenine Dinucleotide Ultraviolet Resonance Raman (UVRR) Spectra at Intracellular Concentration". Applied Spectroscopy 75, nr 8 (2.07.2021): 994–1002. http://dx.doi.org/10.1177/00037028211025575.

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The ultraviolet resonance Raman spectra of the adenine-containing enzymatic redox cofactors nicotinamide adenine dinucleotide and flavin adenine dinucleotide in aqueous solution of physiological concentration are compared with the aim of distinguishing between them and their building block adenine in potential co-occurrence in biological materials. At an excitation wavelength of 266 nm, the spectra are dominated by the strong resonant contribution from adenine; nevertheless, bands assigned to vibrational modes of the nicotinamide and the flavin unit are found to appear at similar signal strength. Comparison of spectra measured at pH 7 with data obtained pH 10 and pH 3 shows characteristic changes when pH is increased or lowered, mainly due to deprotonation of the flavin and nicotinamide moieties, and protonation of the adenine, respectively.

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Pankiewicz, K. W., R. Petrelli, R. Singh i K. Felczak. "Nicotinamide Adenine Dinucleotide Based Therapeutics, Update". Current Medicinal Chemistry 22, nr 34 (19.11.2015): 3991–4028. http://dx.doi.org/10.2174/0929867322666150821100720.

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Kim, Jinhyun, Sahng Ha Lee, Florian Tieves, Caroline E. Paul, Frank Hollmann i Chan Beum Park. "Nicotinamide adenine dinucleotide as a photocatalyst". Science Advances 5, nr 7 (lipiec 2019): eaax0501. http://dx.doi.org/10.1126/sciadv.aax0501.

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Nicotinamide adenine dinucleotide (NAD+) is a key redox compound in all living cells responsible for energy transduction, genomic integrity, life-span extension, and neuromodulation. Here, we report a new function of NAD+ as a molecular photocatalyst in addition to the biological roles. Our spectroscopic and electrochemical analyses reveal light absorption and electronic properties of two π-conjugated systems of NAD+. Furthermore, NAD+ exhibits a robust photostability under UV-Vis-NIR irradiation. We demonstrate photocatalytic redox reactions driven by NAD+, such as O2 reduction, H2O oxidation, and the formation of metallic nanoparticles. Beyond the traditional role of NAD+ as a cofactor in redox biocatalysis, NAD+ executes direct photoactivation of oxidoreductases through the reduction of enzyme prosthetic groups. Consequently, the synergetic integration of biocatalysis and photocatalysis using NAD+ enables solar-to-chemical conversion with the highest-ever-recorded turnover frequency and total turnover number of 1263.4 hour−1 and 1692.3, respectively, for light-driven biocatalytic trans-hydrogenation.

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Pehar, Mariana, Benjamin A. Harlan, Kelby M. Killoy i Marcelo R. Vargas. "Nicotinamide Adenine Dinucleotide Metabolism and Neurodegeneration". Antioxidants & Redox Signaling 28, nr 18 (20.06.2018): 1652–68. http://dx.doi.org/10.1089/ars.2017.7145.

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Rozprawy doktorskie na temat "Nicotinamide adenine dinucleotide"

Moideen, Abdul Nazeer. "Nicotinamide adenine dinucleotide biosynthesis enzymes in rheumatoid arthritis". Thesis, Cardiff University, 2016. http://orca.cf.ac.uk/97161/.

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Introduction: Synovial fibroblasts (SF) display a ‘hyperactive’ phenotype in patients with rheumatoid arthritis (RA). Nicotinamide adenine dinucleotide (NAD+) plays a role in cell metabolism, but may also be a key molecule in maintaining this ‘activated’ phenotype. NAD+ can be synthesised from precursor vitamin molecules, nicotinamide (Nam), nicotinic acid (NA) and Tryptophan (TRP); with their respective phosphoribosyl transferases (NAMPT, NAPRT, QAPRT) and Indoleamine (IDO) being the rate limiting enzymes involved in these pathways. NAMPT and IDO are known to be elevated in RA synovial tissue (ST). However, the expression and regulation of other NAD+ biosynthesis enzymes are unknown. Methods: RA, OA and normal ST were obtained from joints of patients undergoing surgery and expression of NAD+ biosynthesis enzymes were quantified using qPCR. Synovial fibroblasts were cultured and stimulated with 10ng/ml of TNF-α, IL-1β, OSM & IFN- and the expression of NAD+ biosynthesis enzymes were quantified using qPCR. Results: qPCR analyses showed that all NAD+ biosynthesis enzymes tested were constitutively expressed in synovial tissue ex vivo and in vitro, with the exception of NMN adenyltransferase (NMNAT)-3. NAMPT, IDO, QAPRT, NADSYN and NMNAT-2 were all upregulated in RA ST compared to normal tissue, however only NAMPT was significantly upregulated in RA compared to OA and normal, (NAMPT reached statistical significance when patients on anti-TNF therapy were excluded). Moreover, NAMPT was found to be upregulated in ST of young actively developing individuals, decreasing with age. Expression of NAD salvage enzymes, NAMPT and NMNAT-2 in ST correlated with each other and de novo NAD enzymes, IDO, QAPRT, NADSYN and NMNAT-2 were also correlated with each other in ST. NAMPT and IDO were both significantly upregulated in vitro following stimulation with OSM & IFN- but only NAMPT and NMNAT-2 were upregulated following stimulation with TNF-α & IL-1β. NAPRT expression was found to be low in RA ST and there was no upregulation following stimulation by OSM, IFN-, TNF-α & IL-1β. Conclusion: The data presented in this thesis emphasises NAMPT and IDO as a potential therapeutic target in rheumatoid arthritis.

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Stevenson, Eileen C. "The utilisation of fibre-entrapped cells within a novel bioreactor for the production of NADH". Thesis, Queen's University Belfast, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334643.

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Trammell, Samuel A. J. "Novel NAD+ metabolomic technologies and their applications to Nicotinamide Riboside interventions". Diss., University of Iowa, 2016. https://ir.uiowa.edu/etd/3203.

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Nicotinamide adenine dinucleotide (NAD+) is a cofactor in hydride transfer reactions and consumed substrate of several classes of glycohydrolyitc enzymes, including sirtuins. NAD+, its biosynthetic intermediates, breakdown products, and related nucleotides (the NAD metabolome) is altered in many metabolic disorders, such as aging and obesity. Supplementation with the novel NAD+ precursor, nicotinamide riboside (NR), ameliorates these alterations and opposes systemic metabolic dysfunctions in rodent models. Based on the hypothesis that perturbations of the NAD metabolome are both a symptom and cause of metabolic disease, accurate assessment of the abundance of these metabolites is expected to provide insight into the biology of diseases and the mechanism of action of NR in promoting metabolic health. Current quantitative methods, such as HPLC, lack specificity and sensitivity to detect distinct alterations to the NAD metabolome. In this thesis, I developed novel sensitive, accurate, robust liquid chromatography mass spectrometry methodologies to quantify the NAD metabolome and applied these methods to determine the effects of disease states and NR supplementation on NAD+ metabolism. My investigations indicate that NR robustly increases the NAD metabolome, especially NAD+ in a manner kinetically different than any other NAD+ precursor. I provide the first evidence of effective NAD+ supplementation from NR in a healthy, 52 year old human male, suggesting the metabolic promoting qualities of NR uncovered in rodent studies are translatable to humans. During my investigation of NR supplementation, my work establishes an unexpected robust, dramatic increase in deamino–NAD+, NAAD, directly from NR, which I argue could serve as an accessible biomarker for efficacious NAD+ supplementation and the effect of disease upon the NAD metabolome. Lastly, I further establish NR as a general therapeutic against metabolic disorder by detailing its ability to oppose aspects of chronic alcoholism and diabetes mellitus.

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Al, Ghouleh Imad 1977. "The role of nicotinamide adenine dinucleotide phosphate (reduced form) oxidase in endothelial activation in sepsis /". Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115854.

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Septic shock is a leading cause of death in intensive care units. As part of the septic process, the endothelium becomes activated and propagates the septic condition. It has become evident that reactive oxygen species (ROS) are involved in the signaling of mediators of sepsis, such as tumor necrosis factor-alpha (TNF-alpha) and the lipopolysaccharide coating of gram-negative bacteria (LPS). An important source of these ROS is NADPH oxidase, which is a ubiquitously expressed enzyme complex that also exists in endothelial cells (EC). We showed that O2- from NADPH oxidase was important for LPS, as well as TNF-alpha, induction of two markers of an activated endothelium, interleukin-8 (IL-8) and intercellular adhesion molecule-1 (ICAM-1) in human umbilical vein endothelial cells (HUVEC).
Expression of a gene can be increased by a rise in transcription as well as post-transcriptional changes, such as mRNA stability modifications. We assessed the role of NADPH oxidase in this process and found a complex interaction. Although LPS increases IL-8 transcription, it also destabilizes IL-8 mRNA in a p38 and extracellular signal-regulated kinase (ERK) MAPK dependent manner, which was only evident after blocking NADPH oxidase. This regulation involved the mRNA de-stabilizing factor tristetraprolin (TTP). In contrast, TNF-alpha enhanced the stability of IL-8, IL-6 and ICAM-1 mRNA in a p38 MAPK dependent, but NADPH oxidase independent manner. Furthermore, LPS did not have an effect on mRNA stability of IL-6 or ICAM-1 in our system. Thus, we conclude from our studies that the NAPDH oxidase is important for the induction of inflammatory molecules in LPS and TNF-alpha treated EC and is also involved in mRNA stability regulation of these molecules in a signal and gene specific fashion.

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Pergolizzi, Giulia. "Novel derivatives of nicotinamide adenine dinucleotide (NAD) and their biological evaluation against NAD-consuming enzymes". Thesis, University of East Anglia, 2012. https://ueaeprints.uea.ac.uk/42447/.

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Nicotinamide adenine dinucleotide (β-NAD+) is a primary metabolite involved in fundamental biological processes. Its molecular structure with characteristic functional groups, such as the quaternary nitrogen of the nicotinamide ring, and the two high-energy pyrophosphate and nicotinamide N-glycosidic bonds, allows it to undergo different reactions depending on the reactive moiety. Well known as a redox substrate owing to the redox properties of the nicotinamide ring, β-NAD+ is also fundamental as a substrate of NAD+-consuming enzymes that cleave either high-energy bonds to catalyse their reactions. In this study, a panel of novel adenine-modified NAD+ derivatives was synthesized and biologically evaluated against different NAD+-consuming enzymes. The synthesis of NAD+ derivatives, modified in position 2, 6 or 8 of the adenine ring with aryl/heteroaryl groups, was accomplished by Suzuki-Miyaura cross-couplings. Their biological activity as inhibitors and/or non-natural substrates was assessed against a selected range of NAD+-consuming enzymes. The fluorescence of 8-aryl/heteroaryl NAD+ derivatives allowed their use as biochemical probes for the development of continuous biochemical assays to monitor NAD+-consuming enzyme activities. The introduction of different substituents in position 8 on the adenine ring allowed the modulation of their fluorescence, resulting in the development of more sensitive and alternative probes compared to the known fluorophore ε-NAD+. The different substitutions introduced on the adenine ring also allowed us to probe the active site of an NAD+-dependent bacterial DNA ligase. The selective activity of 8-aryl/heteroaryl NAD+ derivatives against different NAD+-consuming enzymes offers excellent opportunities for their application as tool compounds in in-vitro/in-vivo studies, and as inhibitor templates for drug discovery.

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Balico, Laís de Lourdes de Lima. "Caracterização molecular e bioquímica de um transportador mitocondrial de nicotinamida adenina dinucleotídeo de Aspergillus fumigatus". Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/60/60135/tde-17042015-135749/.

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O A. fumigatus é um fungo saprofítico e tornou-se um dos principais agente patogênico oportunista em pacientes imunossuprimidos. Estudos prévios em nosso laboratório foi demonstrado que em mitocôndrias de P. brasiliensis e de A. fumigatus, o NAD+ era capaz de induzir a formação de potencial de membrana mitocondrial, o qual podia ser dissipado por FCCP, sugerindo a presença de um transportador de NAD+/NADH, conforme havia sido descrito em S. cerevisiae. Através de ferramentas de bioinformática, foi identificado no Aspergillus Gene Database, uma sequência com 32% de identidade com o gene ndt1p de S. cerevisiae. A sequência de cDNA, contendo 1.194 pb foi obtida usando PCR-Overlaping e clonada em vetor pGEM®-T Easy. Em seguida, a sequência foi subclonada em vetor de expressão pET28-a(+) e expressa em E. coli BL21(DE3). A proteína recombinante foi purificada a partir dos corpos de inclusão e sua identidade confirmada por espectrometria de massas e por Western Blotting usando anticorpo anti-His-tag. A proteína recombinante foi utilizada para produção de anticorpo policlonal anti-Ndt1 em coelho. Para expressão em levedura, o cDNA do gene ndt1 de A. fumigatus foi subclonado em vetor pYES2 e as leveduras S. cerevisiae ?ndt1?ndt2 foram transformadas. Foi realizada a curva de crescimento e indução da expressão da proteína recombinante Ndt1, a presença da proteína foi detectada utilizando anticorpo policlonal anti-Ndt1 após 16 horas de expressão. Nesse período foi verificado que as leveduras estavam em fase de crescimento exponencial. A cepa duplo mutante apresenta uma taxa de crescimento menor quando comparada com a cepa expressando a proteína recombinante quando crescidas em meio fermentável. As mitocôndrias isoladas de ambas as cepas foram submetidas à medida do potencial de membrana onde apresentavam acoplamento entre a oxidação de substratos e a fosforilação oxidativa. Além disso, ficou evidenciado que na cepa expressando a proteína recombinante, NAD+ induziu a formação de um potencial de membrana maior que na cepa controle. O transporte de NAD+ foi realizado e demonstrou que a cepa expressando a proteína Ndt1 tinha um aumento na fluorescência de NADH, mostrando que NAD+ foi capaz de entrar na matriz mitocondrial e posteriormente ser reduzido a NADH por enzimas da matriz mitocondrial. A determinação da produção de espécies reativas de oxigênio foi realizada utilizando as sondas fluorescentes CM-H2DCFDA e MitoSox Red em esferoplastos da levedura S. cerevisiae. Ambos experimentos não houve diferença significativa entre a cepa expressando a proteína Ndt1 e a cepa controle. As proteínas carboniladas foram determinadas utilizando anticorpo anti-DNP, após a reação com dinitrofenilhidrazona e não há diferença significativa entre as cepas. Finalmente, para confirmação da localização celular da proteína Ndt1, os esferoplastos de S. cerevisiae foram submetidos à microscopia confocal, onde ficou evidenciado a co-localização da proteína Ndt1 com as mitocôndrias na cepa de S. cerevisiae transformada com a construção pYES/ndt1, o mesmo perfil não foi observado na cepa ?ndt1?ndt2.
The A. fumigatus is a saprophytic fungus and is a major opportunistic pathogen in immunosuppressed patients. Previous studies in our lab has showed that mitochondrias of the P. brasiliensis and A. fumigatus, NAD+ is able to induce the formation of mitochondrial membrane potential, which could be dissipated by FCCP, suggesting the presence of a NAD+/NADH carrier as described in S. cerevisiae. Using bioinformatics tools, it was identified in Aspergillus Gene database a sequence containing 32% of identity with the gene ndt1p of S. cerevisiae. A fragment of cDNA was obtained from the ndt1p mRNA sequence, containing 1194 bp by using PCR-overlaping and cloned in pGEM®-T Easy vector. Then, the sequence was subcloned in pET28-a(+) vector and expressed in E. coli BL21 (DE3). The recombinant protein was purified from inclusion bodies and the identity confirmed by mass spectrometry and by Western Blotting using anti-His-tag antibody. The recombinant protein was used to produce polyclonal antibody anti-Ndt1 in rabbit. For expression in yeast, the ndt1 cDNA of A. fumigatus was subcloned into pYES2 vector and the yeast S. cerevisiae ?ndt1?ndt2 were transformed. Growth curve and induction of the recombinant protein expression Ndt1 was performed and the protein was detected using a polyclonal anti-Ndt1 antibody after 16 hours of expression. During this period it was found that the yeast were in exponential growth phase. The double mutant strain shows a slower growth rate compared to the strain expressing the recombinant protein growth rate when grown in fermentable medium. The isolated mitochondria from both strains were subjected to measurement of the membrane potential which showed coupling between substrate oxidation and oxidative phosphorylation. Furthermore, these measurements evidenced that the strain expressing the recombinant protein NAD+ induced the formation of a membrane potential larger than the control strain. The transport NAD+ was evaluated and showed that the strain expressing the protein Ndt1 has an increase in NADH fluorescence, indicating that NAD+ was able to enter into the mitochondrial matrix and then reduced to NADH by enzymes from the matrix. The determination of the production of reactive oxygen species was performed using the fluorescent probe CM-H2DCFDA and MitoSox Red in spheroplasts of the yeast S. cerevisiae. Both experiments showed no significant difference between the strain expressing Ndt1 protein and strain control. The carbonylated proteins levels were checked using anti-DNP, after the reaction with dinitrophenylhydrazone and there is no significant difference between the strains. Finally, to confirm the cellular localization of the protein Ndt1, spheroplasts of S. cerevisiae were subjected to confocal microscopy, which evidenced the co-location of Ndt1 protein with mitochondria in S. cerevisiae strain transformed with the construction pYES/ndt1. This same profile was not observed in strain ?ndt1?ndt2.

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Preyat, Nicolas. "Tumor necrosis factor-induced necroptosis is regulated by nicotinamide adenine dinucleotide in a sirtuin-dependent manner". Doctoral thesis, Universite Libre de Bruxelles, 2013. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209470.

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Nicotinamide adenine dinucleotide (NAD+) represents a long-known key molecule in cellular metabolism. It was initially identified for its ability to convey electrons and protons between redox partners in multiple bioenergetic and biosynthetic reactions. In addition, NAD+ also serves as a substrate for NAD+-consuming enzymes such as sirtuins and poly ADP-ribose polymerases (PARPs). These latter enzymes catalyze dynamic post-translational modifications that control virtually every signaling pathway orchestrating cell fate. The aim of this work was to analyze the role of NAD+ in the context of programmed cell death mechanisms.

Our findings indicate that NAD+ is protective against DNA damage-induced cell death and FAS-induced apoptosis, while, unexpectedly, it promotes TNF-induced necroptosis, a regulated form of necrosis. Indeed raising NAD+ cellular levels sensitized culture cells to necroptosis, while NAD+ depletion protected cells from this form of cell death. Furthermore, specific silencing of NAD+-dependent sirtuins was also found to be protective against TNF-induced necroptosis. Consistently, a pharmacological pan-sirtuin inhibitor called cambinol protected cells from necroptosis. Then, as necroptosis represents a back-up mechanism that may have evolved in response to viral pathogens expressing anti-apoptotic proteins, we demonstrated in an in vitro model mimicking viral infection that pharmacological sirtuin inhibition protected cells from poly I:C-induced necroptotic cell death. In vivo, we demonstrated that cambinol partially protected kidney from necrosis after ischemia/reperfusion. We have also shown that enhancing liver NAD+ concentration via isonicotinamide increases the susceptibility of mice to systemic inflammatory response syndrome (SIRS). Moreover, our preliminary data show that isonicotinamide substantially improves the ability of cyclophosphamide to trigger the rejection of the murine mastocytoma P815 tumor cell line.

Collectively, our observations point to a role for NAD+ in the control of necroptosis in a sirtuin-dependent manner. These observations may bear relevance to the better understanding of the pathophysiological consequences of excessive production of the pro-inflammatory cytokine TNF and the control of viral infections and tumor progression/immunotherapy. &
Doctorat en Sciences
info:eu-repo/semantics/nonPublished

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Smyth, Lisa M. "The nicotinamide adenine dinucleotide (NAD)/cyclic ADP-ribose/ADP-ribose system, new to the peripheral synapse". abstract and full text PDF (free order & download UNR users only), 2005. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3210943.

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BERTRAND, MARTINE. "Photoreduction du nicotinamide adenine dinucleotide phosphate par des etioplastes de haricot (phaseolus vulgaris l. Var commodore)". Paris 6, 1988. http://www.theses.fr/1988PA066079.

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Brunnbauer, Philipp [Verfasser]. "On the measurement and systemic relevance of extracellular nicotinamide adenine dinucleotide in human plasma / Philipp Brunnbauer". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2020. http://d-nb.info/1206185988/34.

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Książki na temat "Nicotinamide adenine dinucleotide"

Jackson, J. B. The proton-translocating nicotinamide adenine dinucleotide transhydrogenase. London: New York, 1991.

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Rissiek, Björn, Andreas H. Guse, Sahil Adriouch i Santina Bruzzone, red. The Versatile Role of Nicotinamide Adenine Dinucleotide in Immunity. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-085-7.

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Części książek na temat "Nicotinamide adenine dinucleotide"

Andrews, Anne M., Greg A. Gerhardt, Lynette C. Daws, Mohammed Shoaib, Barbara J. Mason, Charles J. Heyser, Luis De Lecea i in. "Nicotinamide Adenine Dinucleotide". W Encyclopedia of Psychopharmacology, 877. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1030.

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Clausen, Torben, José Luis Trejo, Mark P. Mattson, Alexis M. Stranahan, Joanna Erion, Rosa Maria Bruno, Stefano Taddei i Melinda M. Manore. "Nicotinamide Adenine Dinucleotide". W Encyclopedia of Exercise Medicine in Health and Disease, 645. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2763.

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Ziegler, Mathias. "Nicotinamide Adenine Dinucleotide (NAD)". W Encyclopedia of Biophysics, 1710–12. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-16712-6_42.

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Riley, David S. "Nicotinamide adenine dinucleotide (NAD)". W Materia Medica of New and Old Homeopathic Medicines, 143–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-25292-1_48.

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Braidy, Nady, Anne Poljak i Perminder Sachdev. "Nicotinamide Adenine Dinucleotide (NAD+) in Aging". W Encyclopedia of Gerontology and Population Aging, 1–10. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-69892-2_1035-1.

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Braidy, Nady, Anne Poljak i Perminder Sachdev. "Nicotinamide Adenine Dinucleotide (NAD+) in Aging". W Encyclopedia of Gerontology and Population Aging, 3496–505. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-22009-9_1035.

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Jiang, Jinxia, Min Feng, Annemarie Jacob, Lin Z. Li i He N. Xu. "Optical Redox Imaging Differentiates Triple-Negative Breast Cancer Subtypes". W Advances in Experimental Medicine and Biology, 253–58. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-48238-1_40.

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AbstractTriple-negative breast cancer (TNBC) is a highly diverse group of cancers with limited treatment options, responsible for about 15% of all breast cancers. TNBC cells differ from each other in many ways such as gene expression, metabolic activity, tumorigenicity, and invasiveness. Recently, many research and clinical efforts have focused on metabolically targeted therapy for TNBC. Metabolic characterization of TNBC cell lines can facilitate the assessment of therapeutic effects and assist in metabolic drug development. Herein, we used optical redox imaging (ORI) techniques to characterize TNBC subtypes metabolically. We found that various TNBC cell lines had differing redox statuses (levels of reduced nicotinamide adenine dinucleotide (NADH), oxidized flavin adenine dinucleotide (FAD), and the redox ratio (FAD/(NADH+FAD)). We then metabolically perturbed the cells with mitochondrial inhibitors and an uncoupler and performed ORI accordingly. As expected, we observed that these TNBC cell lines had similar response patterns to the metabolic perturbations. However, they exhibited differing redox plasticity. These results suggest that subtypes of TNBC cells are different metabolically and that ORI can serve as a sensitive technique for the metabolic profiling of TNBC cells.

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Bell, Charles E., i David Eisenberg. "Crystal Structure of Diphtheria Toxin Bound to Nicotinamide Adenine Dinucleotide". W Advances in Experimental Medicine and Biology, 35–43. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4419-8632-0_4.

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Gorton, L., B. Persson, P. D. Hale, L. I. Boguslavsky, H. I. Karan, H. S. Lee, T. A. Skotheim, H. L. Lan i Y. Okamoto. "Electrocatalytic Oxidation of Nicotinamide Adenine Dinucleotide Cofactor at Chemically Modified Electrodes". W ACS Symposium Series, 56–83. Washington, DC: American Chemical Society, 1992. http://dx.doi.org/10.1021/bk-1992-0487.ch006.

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Phadke, Ratna S., Rajesh Manchanda i Girjesh Govil. "Immobilization of Nicotinamide Adenine Dinucleotide: Implications in Molecular Electronics and Bioengineering". W Molecular Electronics, 289–95. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4615-7482-8_30.

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Streszczenia konferencji na temat "Nicotinamide adenine dinucleotide"

Hristovska, Talija, Kosta Petrović, Marko Cincović, Branislava Belić, Maja Došenović Marinković, Radojica Đoković, Miloš Petrović i Dražen Kovačević. "UTICAJ APLIKACIJE NIACINA NA VREDNOST NJEGOVIH VITAMERA U KRVI KRAVA U RANOJ LAKTACIJI". W XXVII savetovanje o biotehnologiji. University of Kragujevac, Faculty of Agronomy, 2022. http://dx.doi.org/10.46793/sbt27.263h.

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Vitamin niacin is of great importance for energy metabolism. Physiological niacin is incorporated into the coenzyme nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP). The aim of this study was to determine the concentration of NAD and NADP in the blood of cows during the application of niacin in the peripartum period. The value of these vitamins depends on the peripartum week, regardless of the constant exogenous source of niacin.

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Sharma, Ashutosh. "Novel reduced nicotinamide adenine dinucleotide optical sensor". W OE/LASE '94, redaktorzy James A. Harrington, David M. Harris, Abraham Katzir i Fred P. Milanovich. SPIE, 1994. http://dx.doi.org/10.1117/12.180770.

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Ghukasyan, Vladimir V., i Fu-Jen Kao. "Monitoring Cellular Metabolism with Fluorescence Lifetime of Reduced Nicotinamide Adenine Dinucleotide". W Asia Communications and Photonics Conference and Exhibition. Washington, D.C.: OSA, 2009. http://dx.doi.org/10.1364/acp.2009.fe4.

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Sipos, Áron, Rita Nagypál, Ferenc Sarlós i Géza I. Groma. "Vibrational relaxation demonstrated in nicotinamide adenine dinucleotide applying machine learning based analysis". W IX. Szimpózium a hazai kvantumelektronikai kutatások eredményeiről. Szeged: Szegedi Tudományegyetem Természettudományi és Informatikai Kar Fizikai Intézet, 2021. http://dx.doi.org/10.14232/kvantumelektronika.9.30.

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Sharma, Ashutosh. "Novel fluorescence method for development of nicotinamide adenine dinucleotide and secondary biosensors". W OE/LASE '94, redaktorzy James A. Harrington, David M. Harris, Abraham Katzir i Fred P. Milanovich. SPIE, 1994. http://dx.doi.org/10.1117/12.180768.

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Schramm, Werner, Mathias Nittka, Wolfgang Hoehne, Heinz D. Kronfeldt i Joerg Rauschenberg. "Registration of damages of endothelial cell cultures by beta-nicotinamide adenine dinucleotide (NADH) fluorescence". W International Symposium on Biomedical Optics Europe '94, redaktorzy Hans-Jochen Foth, Aaron Lewis, Halina Podbielska, Michel Robert-Nicoud, Herbert Schneckenburger i Anthony J. Wilson. SPIE, 1995. http://dx.doi.org/10.1117/12.200883.

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Pan, Fu-shih, Stephen Chen, Robert A. Mintzer, Chin-Tu Chen i Paul Schumacker. "Studies of yeast cell oxygenation and energetics by laser fluorometry of reduced nicotinamide adenine dinucleotide". W Midwest - DL tentative, redaktorzy Rudolph P. Guzik, Hans E. Eppinger, Richard E. Gillespie, Mary K. Dubiel i James E. Pearson. SPIE, 1991. http://dx.doi.org/10.1117/12.25761.

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Moreno-Vinasco, Liliana, Saad Sammani, Hector Quijada, Jessica Siegler, Ting Wang, Eleftheria Letsiou, Rafael Zaidi, Joe Messana, Roberto F. Machado i Joe G. N. Garcia. "Extracellular Nicotinamide Adenine Dinucleotide (NAD) Is Protective In Acute Lung Injury (ALI) And ALI-Ventilator-Induced Lung Injury (VILI)". W American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5455.

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Gehrke, Iris, Armando Poeppl, James Johnston, Spencer B. Gibson i Versha Banerji. "Abstract 1906: Differential downstream effects of nicotinamide adenine dinucleotide (NAD) salvage pathway-inhibition in chronic lymphocytic leukemia (CLL) and multiple myeloma (MM)." W Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1906.

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Gonzales, Joyce, Boris A. Gorshkov, Paul Biddinger, Stephen Black, Alexander D. Verin i Nagavedi S. Umapathy. "Beta Nicotinamide Adenine Dinucleotide (ß-NAD) Protects Lung Endothelial Cell Barrier Dysfunction In Acute Lung Injury/Acute Respiratory Distress Syndrome (ALI/ARDS)". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2670.

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