Relevant bibliographies by topics / Purine nucleotides

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Academic literature on the topic 'Purine nucleotides'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Purine nucleotides"

1

Tomlinson, Patricia Tolson, and Carol J. Lovatt. "Nucleotide Metabolism in ‘Washington’ Navel Orange Fruit: I. Pathways of Synthesis and Catabolism." Journal of the American Society for Horticultural Science 112, no. 3 (May 1987): 529–35. http://dx.doi.org/10.21273/jashs.112.3.529.

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Abstract The capacity of ‘Washington’ navel orange fruit [Citrus sinensis (L.) Osbeck] to synthesize and catabolize purines and pyrimidines was assessed. De novo biosynthesis of purine nucleotide was demonstrated by [14C] bicarbonate incorporation into purine nucleotides, blockage of this process by four known inhibitors, and assimilation of radiolabeled carbon from formate, both carbons of glycine, and carbon-3 of serine into the adenine ring. De novo synthesis of pyrimidines via the orotate pathway in young fruit was demonstrated by incorporation of [14C] bicarbonate and [6-14C]orotic acid into uridine nucleotides, release of 14CO2 from [7-14C]orotic acid, and blockage of these processes by 6-azauridine. Synthesis of purine and pyrimidine nucleotides via salvage reactions was demonstrated by incorporation of radiolabeled bases and ribonucleosides into nucleotides and into nucleic acids. Release of 14CO2 from radiolabeled adenine, adenosine, hypoxanthine, and xanthine, uric acid, urea (purines), uracil, and uridine (pyrimidines) provided evidence the pathways for catabolism (degradation) of purines and pyrimidines in navel orange fruit are similar to those found in microorganisms and animal tissues. To the best of our knowledge, this report is the first to assess the capacity of anabolic and catabolic pathways of purine and pyrimidine nucleotide metabolism in fruit of any species. De novo synthetic activities in orange fruit permit increases in the pools of purine and pyrimidine nucleotides using simple precursors. Further, the patterns of salvage and catabolism suggest riboside pools are reused predominantly as nucleotides, while the majority of base pools are degraded to permit recycling of carbon and nitrogen into other metabolites.
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Walsh, M. J., A. Sanchez-Pozo, and N. S. Leleiko. "A regulatory element is characterized by purine-mediated and cell-type-specific gene transcription." Molecular and Cellular Biology 10, no. 8 (August 1990): 4356–64. http://dx.doi.org/10.1128/mcb.10.8.4356-4364.1990.

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Purines and purine nucleotides were found to affect transcription of the hypoxanthine-guanine phosphoribosyltransferase (HPRT) gene in whole nuclei isolated from intestinal mucosa of adult rats fed a purine- and purine nucleotide-free diet. Nuclear run-on transcription assays, performed on whole nuclei from different tissues and cell types, identified an intestine-specific decrease in the overall incorporation of [alpha-32P]UTP in HPRT transcripts from intestinal epithelial cell nuclei when exogenous purines or purine nucleotides were omitted from either the diet or culture medium. Using a 990-base-pair genomic fragment that contains the 5'-flanking region from the HPRT gene, we generated plasmid constructs with deletions, transfected the DNA into various cell types, and assayed for chloramphenicol acetyltransferase (CAT) reporter activity in vitro. We determined that an element upstream from the putative transcriptional start site is necessary to maintain the regulatory response to purine and nucleotide levels in cultured intestinal epithelial cells. These results were tissue and cell type specific and suggest that in the absence of exogenous purines, the presence of specific factors influences transcriptional initiation of HPRT. This information provides evidence for a mechanism by which the intestinal epithelium, which has been reported to lack constitutive levels of de novo purine nucleotide biosynthetic activity, could maintain and regulate the salvage of purines and nucleotides necessary for its high rate of cell and protein turnover during fluctuating nutritional and physiological conditions. Furthermore, this information may provide more insight into regulation of the broad class of genes recognized by their lack of TATA and CCAAT box consensus sequences within the region proximal to the promoter.
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Walsh, M. J., A. Sanchez-Pozo, and N. S. Leleiko. "A regulatory element is characterized by purine-mediated and cell-type-specific gene transcription." Molecular and Cellular Biology 10, no. 8 (August 1990): 4356–64. http://dx.doi.org/10.1128/mcb.10.8.4356.

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Purines and purine nucleotides were found to affect transcription of the hypoxanthine-guanine phosphoribosyltransferase (HPRT) gene in whole nuclei isolated from intestinal mucosa of adult rats fed a purine- and purine nucleotide-free diet. Nuclear run-on transcription assays, performed on whole nuclei from different tissues and cell types, identified an intestine-specific decrease in the overall incorporation of [alpha-32P]UTP in HPRT transcripts from intestinal epithelial cell nuclei when exogenous purines or purine nucleotides were omitted from either the diet or culture medium. Using a 990-base-pair genomic fragment that contains the 5'-flanking region from the HPRT gene, we generated plasmid constructs with deletions, transfected the DNA into various cell types, and assayed for chloramphenicol acetyltransferase (CAT) reporter activity in vitro. We determined that an element upstream from the putative transcriptional start site is necessary to maintain the regulatory response to purine and nucleotide levels in cultured intestinal epithelial cells. These results were tissue and cell type specific and suggest that in the absence of exogenous purines, the presence of specific factors influences transcriptional initiation of HPRT. This information provides evidence for a mechanism by which the intestinal epithelium, which has been reported to lack constitutive levels of de novo purine nucleotide biosynthetic activity, could maintain and regulate the salvage of purines and nucleotides necessary for its high rate of cell and protein turnover during fluctuating nutritional and physiological conditions. Furthermore, this information may provide more insight into regulation of the broad class of genes recognized by their lack of TATA and CCAAT box consensus sequences within the region proximal to the promoter.
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4

Rosiers, Christine Des, Stephan Nees, and Eckehart Gerlach. "Purine metabolism in cultured aortic and coronary endothelial cells." Biochemistry and Cell Biology 67, no. 1 (January 1, 1989): 8–15. http://dx.doi.org/10.1139/o89-002.

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Purine salvage pathways in cultured endothelial cells of macrovascular (pig aorta) and microvascular (guinea pig coronary system) origin were investigated by measuring the incorporation of radioactive purine bases (adenine or hypoxanthine) or nucleosides (adenosine or inosine) into purine nucleotides. These precursors were used at initial extracellular concentrations of 0.1, 5, and 500 μM. In both types of endothelial cells, purine nucleotide synthesis occurred with all four substrates. Aortic endothelial cells salvaged adenine best among purines and nucleosides when applied at 0.1 μM. At 5 and 500 μM, adenosine was the best precursor. In contrast, microvascular endothelial cells from the coronary system used adenosine most efficiently at all concentrations studied. The synthetic capacity of salvage pathways was greater than that of the de novo pathway. As measured using radioactive formate or glycine, de novo synthesis of purine nucleotides was barely detectable in aortic endothelial cells, whereas it readily occurred in coronary endothelial cells. Purine de novo synthesis in coronary endothelial cells was inhibited by physiological concentrations of purine bases and nucleosides, and by ribose or isoproterenol. The isoproterenol-induced inhibition was prevented by the β-adrenergic receptor antagonist propranolol. The end product of purine catabolism in aortic endothelial cells was found to be hypoxanthine, whereas coronary endothelial cells degraded hypoxanthine further to xanthine and uric acid, a reaction catalyzed by the enzyme xanthine dehydrogenase.Key words: purine metabolism, aortic endothelial cells, coronary endothelial cells, β-adrenergic receptor.
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Arabadjis, P. G., P. C. Tullson, and R. L. Terjung. "Purine nucleoside formation in rat skeletal muscle fiber types." American Journal of Physiology-Cell Physiology 264, no. 5 (May 1, 1993): C1246—C1251. http://dx.doi.org/10.1152/ajpcell.1993.264.5.c1246.

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To determine the capacity for purine nucleotide degradation among skeletal muscle fiber types, we established energy-depleted conditions in muscles of the rat hindlimb by inducing muscle contraction during ischemia. After 5, 10, 15, or 20 min of ischemic contractions, representative muscle sections were freeze-clamped and analyzed for purine nucleotides, nucleosides, and bases. Fast-twitch muscle sections accumulated about fourfold more IMP than the slow-twitch red soleus muscle. Inosine begins to accumulate at < 0.5 mumol/g IMP in slow-twitch muscle and at approximately 2 mumol/g IMP in fast-twitch muscle. This suggests that inosine is formed intracellularly by 5'-nucleotidase acting on IMP and that the activity and/or substrate affinity of the 5'-nucleotidase present in slow-twitch muscle may be higher than in fast-twitch muscle. At similar concentrations of precursor IMP, slow-twitch muscle has a greater capacity for purine nucleoside formation and should be more dependent on salvage and de novo synthesis of purine for the maintenance of muscle adenine nucleotides. Fast-twitch muscles are better able to retain IMP for subsequent reamination due to their lower capacity to degrade IMP to inosine.
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Marutyan, Seda V., Gayane H. Petrosyan, Syuzan A. Marutyan, Liparit A. Navasardyan, and Armen H. Trchounian. "INFLUENCE OF X-RAY AND MICROWAVE RADIATION ON DEAMINATION OF PURINE NUCLEOTIDES IN YEAST CELLS CANDIDA GUILLIERMONDII NP-4." IZVESTIYA VYSSHIKH UCHEBNYKH ZAVEDENII KHIMIYA KHIMICHESKAYA TEKHNOLOGIYA 62, no. 2 (February 7, 2019): 48–52. http://dx.doi.org/10.6060/ivkkt.20196202.5894.

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In metabolism of living cells a key role play purine nucleotides which cells can be supplied either by de novo synthesis from lower molecular weight precursors, or by alternate ways of nucleotide synthesis or so-called "nucleotide salvage pathways", which allow reusing of intermediate products of nucleotide metabolism in nucleotide synthesis. This way is important in the post-stress repair period, saving energy and substrates in the repairing cells. Purine nucleotides are allosteric inhibitors of enzymes of nucleotide salvage pathways, therefore the increase in their catabolism leads to a decrease of their amount in the cells, which contributes to the intensive work of the nucleotide salvage pathways and provides substrates for DNA synthesis. Investigation of deamination of purine nucleotides in yeasts Candida guilliermondii NP-4 irradiated with X-rays, millimeter and decimeter electromagnetic waves, as well as after post-radiation incubation of cells has been realized. It has been shown that under the influence of X-ray and microwave irradiation in yeasts, the intensity of deamination of purine nucleotide-polyphosphates - ADP, ATP, GDF and GTP, has changed, which in all probability is an adaptive mechanism in the repair of yeasts after irradiation, provides the work of nucleotide salvage pathways, and can be associated with the metabolism of these compounds.
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Ahmed, A. U., J. Shireman, F. Atashi, M. Saathoff, E. Ali, G. Lee, C. Park, et al. "OS6.1 Targeting Purine Metabolism to Overcome Therapeutic Resistance in Glioblastoma." Neuro-Oncology 21, Supplement_3 (August 2019): iii12. http://dx.doi.org/10.1093/neuonc/noz126.039.

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Abstract BACKGROUND A distinguishing characteristic of all cancers is uncontrolled cell division, and they require additional nucleotide bases such as purines, the building blocks of DNA and RNA, to sustain their uncontrolled growth. Purines can be synthesized from scratch by de novo pathway or salvaged by recycling surrounding nucleotides that are released by hydrolytic degradation. Even though the central nervous system (CNS), as well as CNS associated malignancies like glioblastoma (GBM), rely more heavily on the salvage pathway due to its energy efficiency, its precious role in promoting chemoresistance and GBM recurrence is yet to be elucidated. MATERIAL AND METHODS We have examined the role of purine biosynthesis in GBM by using stable isotope tracing analysis as well as utilizing a knockdown (KD) system to investigate its effect on i) DNA damage response during temozolomide (TMZ) therapy, ii) tumor engraftment and iii) therapeutic responses in vivo. RESULTS Through gene expression and protein-protein interaction analysis, we have identified ARL13B, member of ADP-ribosylation factor-like protein family, as a novel regulator of the purine biosynthesis pathway in GBM. ARL13B can physically interacting with the inosine monophosphate dehydrogenase 2 (IMPDH2), a key rate-limiting enzyme for purine biogenesis. Isotope tracer analysis under normal physiological conditions revealed that during TMZ treatment, salvage recycling activity was decreased by 50% while de novo pathway activity remains unchanged. In contrast, TMZ treatment of ARL13B knock-out cells results in a ~50% decrease in de novo pathway activity (p-value=0.004), whereas purine salvage pathway activity is upregulated ~6-fold (p-value <0.0001). ARL13B knockdown cells treated with TMZ show a robust increase in DNA double-strand breaks compared to control cells exposed to TMZ, as demonstrated by gH2X staining. Mice orthotopically engrafted with KD cells experience prolonged survival relative to mice engrafted with unmodified cells. CONCLUSION We propose that ARL13B-IMPDH2 interaction has two consequences: i) augmentation of de novo purine biosynthesis activity, and ii) inhibition of nucleotide recycling. The increasing de novo purine biosynthesis during TMZ therapy helps GBM cells reduce the recycling of nucleotides via the salvage pathway that have been modified as a result of TMZ alkylation. This, in turn, protects the cells from deleterious effects of incorporating modified nucleotides into newly-synthesized DNA while maintaining a supply of purine building blocks to support uncontrolled proliferation. Our results indicate that the interaction of ARL13B-IMPDH2 functions as a purine biosynthesis regulator that could be targeted for increasing efficacy of TMZ treatment of GBM. ​
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Tomlinson, Patricia Tolson, and Carol J. Lovatt. "Nucleotide Metabolism in ‘Washington’ Navel Orange Fruit: II. Pathway Capacities During Development." Journal of the American Society for Horticultural Science 112, no. 3 (May 1987): 535–39. http://dx.doi.org/10.21273/jashs.112.3.535.

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Abstract Changes in the capacity of ‘Washington’ navel orange [Citrus sinensis (L.) Osbeck] fruit to synthesize (de novo or by salvage) pyrimidine nucleotides, but not purine nucleotides, appears to be related to the stage of fruit development. De novo pyrimidine synthesis in whole-fruit tissue increased 6-fold during Stage I of development (cell division phase), from 10 nmol [14C]bicarbonate incorporated into uridine nucleotides during 5 hr per g dry weight whole-fruit tissue from ovaries harvested at flower petal drop to 57 nmol for 2-month-old fruit. Capacity of peel tissue to synthesize pyrimidine nucleotides de novo decreased following completion of Stage I, from 43 nmol [14C]bicarbonate incorporated into uridine nucleotides during 5 hr per g dry weight of peel tissue from 2-month-old fruit to 11 nmol for 5-month-old (Stage II) fruit. This decrease was not offset by increased salvage of uridine. Capacity of whole-fruit tissue to synthesize purines de novo increased 3-fold during Stage I. Synthetic capacity of peel tissue from Stage I fruit was half that observed for whole-fruit tissue and did not decrease significantly during Stages II (cell enlargement phase) and III (maturation phase). These observations suggest purine synthetic capacity may not be related to stage of development. Changes in protein or glucose contents, or respiratory activity of peel tissue, could not account for the observed reduction in pyrimidine synthetic capacity. Thus, the reduction observed in synthetic activity was specific for pyrimidine nucleotides. The capacity of fast-growing, 1-month-old fruit (high potential to set) to synthesize or catabolize either pyrimidine or purine nucleotides did not differ from that of slow-growing fruit (low potential to set), suggesting that nucleotide synthesis is not limiting to growth.
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Miller, Jeffrey S., Tereza Cervenka, Jeanne Lund, Ian J. Okazaki, and Joel Moss. "Purine Metabolites Suppress Proliferation of Human NK Cells Through a Lineage-Specific Purine Receptor." Journal of Immunology 162, no. 12 (June 15, 1999): 7376–82. http://dx.doi.org/10.4049/jimmunol.162.12.7376.

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Abstract NK cell proliferation is suppressed in some patients with cancer by unknown mechanisms. Because purine metabolites released into the extracellular space during cell lysis may affect cell function, we hypothesized that these metabolites could serve as feedback regulators of NK cell proliferation. Sorted NK (CD56+/CD3−) cells were incubated with IL-2 (1000 U/ml) in a 4-day thymidine uptake assay with or without 10–10,000 μM of nucleotides. Adenine nucleotides inhibited NK cell proliferation, with ATP = ADP &gt; 5′-adenylylimidodiphosphate &gt; AMP = adenosine; ADP-ribose and nicotinamide adenine dinucleotide, but not nicotinamide or UTP, caused a dose-dependent suppression of thymidine uptake. A total of 100 μM ATP, a concentration that induced a maximal (80%) inhibition of thymidine uptake, did not inhibit cytotoxic activity against K562 targets. Because NK cells retained the ability to lyse K562 targets 4 days after exposure to 500 μM ATP or 1000 μM adenosine, inhibition of thymidine uptake was not due to cell death. Incubation of NK cells with dibutyryl cAMP and forskolin also suppressed thymidine uptake. Cholera toxin and pertussis toxin suppressed NK cell proliferation. Pertussis toxin did not block the adenine nucleotide effects. Further, ATP, but not adenosine or other nucleotides, markedly increased intracellular cAMP in a dose-dependent manner. The ATP-induced increase in cAMP was specific to cytolytic cells, because CD19+ B cells and CD4+ T cells did not increase their intracellular cAMP. These studies demonstrate that NK proliferation is regulated through purine receptors by adenine nucleotides, which may play a role in decreased NK cell activity. The response to adenine nucleotides is lineage-specific.
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Ślepokura, Katarzyna Anna. "Purine 3′:5′-cyclic nucleotides with the nucleobase in asynorientation: cAMP, cGMP and cIMP." Acta Crystallographica Section C Structural Chemistry 72, no. 6 (May 6, 2016): 465–79. http://dx.doi.org/10.1107/s2053229616006999.

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Purine 3′:5′-cyclic nucleotides are very well known for their role as the secondary messengers in hormone action and cellular signal transduction. Nonetheless, their solid-state conformational details still require investigation. Five crystals containing purine 3′:5′-cyclic nucleotides have been obtained and structurally characterized, namely adenosine 3′:5′-cyclic phosphate dihydrate, C10H12N5O6P·2H2O or cAMP·2H2O, (I), adenosine 3′:5′-cyclic phosphate 0.3-hydrate, C10H12N5O6P·0.3H2O or cAMP·0.3H2O, (II), guanosine 3′:5′-cyclic phosphate pentahydrate, C10H12N5O7P·5H2O or cGMP·5H2O, (III), sodium guanosine 3′:5′-cyclic phosphate tetrahydrate, Na+·C10H11N5O7P−·4H2O or Na(cGMP)·4H2O, (IV), and sodium inosine 3′:5′-cyclic phosphate tetrahydrate, Na+·C10H10N4O7P−·4H2O or Na(cIMP)·4H2O, (V). Most of the cyclic nucleotide zwitterions/anions [two from four cAMP present in total in (I) and (II), cGMP in (III), cGMP−in (IV) and cIMP−in (V)] aresynconformers about the N-glycosidic bond, and this nucleobase arrangement is accompanied by Crib—H...Npurhydrogen bonds (rib = ribose and pur = purine). The base orientation is tuned by the ribose pucker. An analysis of data obtained from the Cambridge Structural Database made in the context ofsyn–anticonformational preferences has revealed that among thesynconformers of various purine nucleotides, cyclic nucleotides and dinucleotides predominate significantly. The interactions stabilizing thesynconformation have been indicated. The inter-nucleotide contacts in (I)–(V) have been systematized in terms of the chemical groups involved. All five structures display three-dimensional hydrogen-bonded networks.
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Dissertations / Theses on the topic "Purine nucleotides"

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Payne, Tiffany Anne. "Analysis of dirhenium carboxylate : purine dinucleotide adducts." Scholarly Commons, 2006. https://scholarlycommons.pacific.edu/uop_etds/629.

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The discovery of cisplatin, cis-[pt(NH3)2Cl2], as an anticancer agent in 1969 by Rosenbert and his colleagues sparked interest in the area of metal complexes as chemotherapeutic agents. Anticancer dimetal complexes such as Re2(O2CCH2CH3)2Br4·2H2O are proposed to prevent replication of cancel cells by coordinating to the purine nucleobases in DNA. To investigate the interaction between dimetal compounds and DNA, dirhenium complexes coordinated to purine dinucleotides were isolated and analyzed. LC/MS, HPLC, 1H NMR, and UV-Visible spectroscopy were used to characterized complexes of Re2(O2CR)2X4·2H2O (R = CH3, CH2CH3; X= Cl, Br) with the purine dinucleotides dApG and dGpG. HPLC, UV-Vis, and 1H NMR are used to investigate the aquation of Re2(O2C2H3)2Cl4μ2H2O which may contribute to its biological activity. Upon reaction of Re22C2H3)2Cl4μ2H2O with dApG or dGpG, the intact dirhenium:dinucleotide complex is observed by LC/MS after two days. In both of these reactions, dirhenium:GMP complexes are also observes. 1H NMR studies show the appearance of new resonances in the aromatic region that cannot be attributed to starting material or hydrolyzed DNA fragments. These resonances are proposed to result from the formation of dirhenium:dinucleotide complexes. Additionally, MS spectra support the conclusion that a complex between the dinuclear rhenium complex and the purine dinucleotides of dApG and dGpG is formed after two days. A dirhenium:nucleotide product is also formed as a result of the dinucleotide hydrolysis.
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Worthington, Rebecca A. (Ann). "Structure-function studies of P2X receptors." Thesis, The University of Sydney, 2001. https://hdl.handle.net/2123/27719.

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P2X receptors are fast, ATP-gated cation ion channels. To date seven subtypes of P2X receptors have been cloned and identified, PZXH. The membrane topology of the P2X subunit consists of intracellular amino- and carboxy-termini, two transmembrane spanning domains and a large extracellular loop. Despite similar membrane topology, within this family of receptors the P2X subtypes possess different functional characteristics. They exhibit different sensitivities to agonists and antagonists, are modulated differently by extracellular ions, and have different pore forming abilities. The regions that are responsible for differences in function between P2X subtypes have not been elucidated. This thesis aims to further knowledge regarding the relationship between the structure of the P2X family and differences in the function of the various receptor subtypes. Examination of the primary structure of the P2X receptor family led to the identification of epitope regions suitable for antibody production. This suite of antibodies was tested for specificity and the distribution of P2X receptors was examined in a range of rat tissues and two cell lines. The pathophysiological involvement of the P2X7 receptor was examined in B-CLL patients. Two polymorphisms as well as a loss of function mutation were identified in both normal and leukaemic populations. The site of agonist binding is believed to be within the extracellular loop. Examination of the primary structure of the human cytolytic receptor P2X7 led to the identification of two noncontiguous regions that could potentially be involved in binding ATP. Three amino acid residues that lie within the extracellular loop were targeted and their involvement in ATP binding was determined. Two lysine residues at positions 193 and 31 1 and a proline residue at 210 were each exchanged with alanine. An abolition of function of human receptors with mutations at positions 193 or 311 was observed, consistent with a disruption of the ATP binding domain, although alterations in transduction or gating cannot be dismissed. The P2X receptor appears to be comprised of a trimeric subunit arrangement, and Hill coefficients of between 1 and 3 reported for ATP binding suggest that there is more than one ATP binding site per functional receptor. Modelling of the putative binding cleft of the hP2X7 subunit was performed and the residues important for ATP binding were highlighted. The fimctional trimeric receptor appears to possess three intersubunit ATP binding sites. In an attempt to isolate regions of the extracellular domain that contribute to or control various channel properties, chimaeras between subtypes P2X], P2X4 and P2X7 were constructed and their properties examined. Each of the six chimaeras has been shown to be correctly inserted into the cell membrane and functional. These constructs will continue to be investigated and form the basis for extensive future work.
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Chen, Xue Bin. "Excretion of purine derivatives by sheep and cattle and its use for the estimation of absorbed microbial protein." Thesis, University of Aberdeen, 1989. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=128449.

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The nucleic acids digested by ruminants are essentially of microbial origin. Absorbed purines are extensively degraded and excreted in urine as allantoin, uric acid, xanthine and hypoxanthine. The measurement of the urinary purine derivatives could be used to estimate the uptake of purines and hence that of microbial protein. 1) Automated methods for measurements of purine derivatives were improved. A HPLC method for determining total adenine and guanine was used to measure the purine contents of mixed rumen bacteria and the digestibility of microbial purines in sheep. 2) Endogenous excretions of purine derivatives by sheep and cattle of different physiological states were measured using animals nourished by intragastric infusions of VFA and casein. The species difference in and the effects of changes in protein supply on the endogenous excretion were studied. 3) A microbial nucleic acid extract was infused into the abomasum of lambs at 6 levels. The subsequent urinary excretion of purine derivatives was examined. The results suggested that exogenous purines were utilised by the sheep. A model is proposed to describe the relationship between purine derivative excretion and purine uptake. 4) Allantoin was infused intravenously to sheep and the changes in plasma concentration, nephric tubular re-absorption and urinary excretion of allantoin were studied. Results showed that plasma allantoin was rapidly removed and a constant proportion of the allantoin entering the blood was excreted in urine of sheep. 5) Secretion of allantoin and uric acid into the gut via saliva was quantified in sheep. The possible decomposition of the allantoin in the rumen by microbes in the rumen fluid and in the rumen wall of sheep was examined in vitro and in vivo. Allantoin infused into the rumen or abomasum of sheep and cattle was not recovered in urine. 6) A model for calculation of microbial protein available to sheep is proposed. It is suggested that a different model should be used for cattle. These models were applied in two feeding experiments with sheep and steers.
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Anderson, Crystal Annette. "Reactivity of Re₂(CH₃COO)₂Cl₄·2H₂O with purine DNA dinucleotides." Scholarly Commons, 2005. https://scholarlycommons.pacific.edu/uop_etds/603.

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Covalent binding of dinuclear metal carboxylate compounds to purine DNA nucleobases has been shown to be a source of anticancer activity, and has resulted in intense research to understand the coordination of metal complexes to DNA. This investigation focuses on the formation of dirhenium metal:dinucleotide complexes of purine nucleobases. To our knowledge, complexes formed by the reaction of dinuclear rhenium metal compounds with dinucleotides have not been reported in the literature.
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Rodrigues, Elisandra Márcia. "Estudos moleculares das fosforribosil pirofosfato sintetases." Universidade de São Paulo, 2004. http://www.teses.usp.br/teses/disponiveis/76/76132/tde-18062008-085454/.

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Fosforribosil pirofosfato (PRPP) sintetases são enzimas de central importância em diversas vias metabólicas em todas as células. A enzima PRPP sintetase humana é constituída por um complexo composto de três subunidades catalíticas (PRSI, PRSII e PRSIII) e por proteínas homólogas de 39 e 41 kDa denominadas PRS Associated Proteins (PAPs) cuja função é desconhecida. A importância da PRPP sintetase em humanos, tem sido documentada pela identificação de uma desordem associada ao cromossomo X, resultando em uma atividade aumentada da PRPP sintetase.Em conseqüência se percebem concentrações elevadas na dosagem de ácido úrico, purino nucleotídeos levando ao desenvolvimento de patogenias como a gota e problemas neurológicos. Nesse sentido, realizaram-se estudos moleculares com o complexo enzimático que compõem as PRPP sintetases. Foram obtidos clones do gene hprsI em vetor de expressão pET29a(+) e a enzima foi expressa em bactérias Escherichia coli cepa BL21 (DE3). A proteína recombinante hPRSI foi purificada depois de fracionamento com sulfato de estreptomicina, sulfato de amônio e em coluna cromatográfica de troca iônica. O raio hidrodinâmico e o pI da enzima foram determinados usando respectivamente a técnica de espalhamento dinâmico de luz e o sistema Fast de eletroforese. A enzima foi caracterizada quanto ao seu enovelamento através da técnica de Dicroísmo Circular, apresentando um espectro característico de estrutura enovelada, composta predominantemente por a-hélices. Os genes hprsII e hpap4l-1 que codificam respectivamente para as proteínas hPRSI1 e HPAP41-1 foram clonados no vetor de clonagem pCR4-TOPO. A proteína recombinante hPAP39 foi clonada em vetor pMAL-c2X em fusão com a proteína Maltose Binding Protein (MBP) e expressa em E. coli. A proteína hPAP39 está em fase de purificação e foi submetida ao experimento de Imunoblotting. Investigações estruturais destas enzimas poderão trazer informações fundamentais para o conhecimento da via biossintética, assim como para o desenvolvimento de inibidores específicos visando o tratamento das desordens a elas associadas.
Phosphoribosyl pyrophosphate (PRPP) synthetases are enzymes of central importance in several metabolic pathways in all cells. The enzyme PRPP synthetase complex is composed of three catalytic subunitis (PRSI, PRSII and PRSIII) and homologous 39 and 41 kDa proteins termed PRPP synthetase-Associated Proteins (PAPs) which function is unknown. The importance of PRPP synthetase function in humans has been documented by the identification of an X chromosome-linked disorder associated with super activity of PRPP synthetase. As a consequence uric acid overproduction, purine nucleotide are observed resulting in the development of diseases such as gout and neurodevelopment impairment. In this line, molecular studies were done with the enzyme complex that constitutes the PRPP synthetases. Clones were obtained from the hprsI gene in the pET29a(+) expression vector and the enzyme was expressed in Escherichia coli BL21(DE3) bacterial. The recombinant human PRSI enzyme was purified, after streptomicine and ammonium sulfate fractionation and by anion exchange chromatography. The hPRSI hydrodynamic radius and pI were determined using, respectively, measures of Dynamic Light Scattering (DLS) and isoeletrophocusing electrophoresis. In addition, according to circular dichroism spectroscopy, hPRSI prevalent secondary structure is a-helix. The hprsí and hpap41-1 genes that codify, respectively, to hPRSII and hPAP41-1 proteins were cloned in pCR4-TOPO cloning vector. The recombinant protein hPAP39 was cloned in the pMAl-c2X expression vector in fusion with the Maltose Binding Protein (MBP) and expressed in E.coli. A purification protocol is been establish for the hPAP39 protein and is submitted by imunoblotting technique. Structural investigation of these enzymes will provide information about the biosynthetic pathway de novo of purine nucleotides, as well as to development of specific inhibitors aiming at the treatment of the associated disorders.
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Fong, Yuen Ting. "Quantitative structure retention relationships on using high-performance liquid chromatography." HKBU Institutional Repository, 2003. http://repository.hkbu.edu.hk/etd_ra/426.

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Liu, Jiangqiong. "Kinetic Studies of 6-Halopurine Nucleoside in SNAr Reactions; 6-(Azolyl, Alkylthio and Fluoro)-purine Nucleosides as Substrates for Suzuki Reactions." Diss., CLICK HERE for online access, 2007. http://contentdm.lib.byu.edu/ETD/image/etd1821.pdf.

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Wu, Joe. "HIF-1α in the Heart: Provision of Ischemic Cardioprotection and Remodeling of Nucleotide Metabolism." Digital Commons @ East Tennessee State University, 2014. https://dc.etsu.edu/etd/2450.

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In our studies we found that stabilized expression of HIF-1α in heart led to better recovery of function and less tissue death after 30 minutes of global ischemia, via mechanisms that preserve the mitochondrial polarization. Our group previously showed that HIF-1α conferred ischemic tolerance by allowing cardiomyocytes to use fumarate as an alternative terminal electron acceptor to sustain anaerobic mitochondrial polarization. The source of fumarate was identified as the purine nucleotide cycle (PNC). Here we discovered that HIF-1α upregulates AMP deaminase 2 (AMPD2), the entry point to the PNC. The combination of glycolysis and the PNC may protect the heart's nucleotide resources. We subsequently examined the effects that HIF-1α exerts on nucleotide metabolism in the ischemic heart. We found that HIF-1α expression reduces adenosine accumulation in the ischemic heart. As ATP is depleted during ischemia, AMP accumulates. Our results suggest that AMP metabolism is shunted towards AMPD2 rather than the adenosine producing 5'-nucleotidase pathway. Subsequently, we treated hearts with the PNC inhibitor hadacidin followed by 30 minutes of global ischemia. Inclusion of hadacidin reduced ATP and adenylate energy charge in the hearts. These findings allow us to propose that activity of the PNC prevents the F0F1 ATP synthase from consuming glycolytic ATP in order to maintain mitochondrial polarization during ischemia. Thus, the PNC provides ATP sparing effects and preserves the energy charge in the ischemic heart. The fact that ATP and adenylate energy charge is better preserved during the initial 20 minutes of ischemia in HIF-1α expressing hearts is supportive of our observation that HIF-1α upregulates the PNC. HIF-1α also upregulates adenosine deaminase, which degrades adenosine. The limitation of adenosine accumulation may help HIF-1α expressing hearts avoid toxicity due to chronic adenosine exposure. Finally, we found that HIF-1α induces the expression of the nucleotide salvage enzyme hypoxanthine phosphoribosyl transferase (HPRT). Upon reperfusion HPRT serves to reincorporate the nucleotide degradation product, hypoxanthine, into the adenylate pool and may prevent the production of reactive oxygen species. Collectively, HIF-1α robustly protects the heart from ischemic stress and it upregulates several pathways whose cardioprotective role may extend beyond the remodeling of nucleotide metabolism.
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Barbosa, Sara Isabel Cadinha. "Compostos que interferem no metabolismo dos purina- e pirimidina-nucleótidos: utilização como agentes terapêuticos." Master's thesis, [s.n.], 2015. http://hdl.handle.net/10284/5160.

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Projeto de Pós-Graduação/Dissertação apresentado à Universidade Fernando Pessoa como parte dos requisitos para obtenção do grau de Mestre em Ciências Farmacêuticas
O conteúdo deste trabalho será desenvolvido em dois temas principais, um referente à utilização de compostos que interferem no metabolismo dos purina- e pirimidinanucleótidos como agentes antineoplásicos e outro referente à sua utilização como agentes antivirais. A síntese dos nucleótidos envolve a construção de ácidos nucleicos e a inserção dos derivados de nucleótidos noutras vias bioquímicas, sendo responsável por inúmeras funções do metabolismo celular. Existem patologias que envolvem enzimas essenciais do metabolismo dos nucleótidos, o que levou à síntese de novos fármacos. As doenças oncológicas continuam a matar milhares de pessoas e um tratamento eficaz e com sucesso tem sido um desafio. O mesmo se passa com algumas infeções virais, nomeadamente infeções provocadas pelo HIV. Para contornar os obstáculos enfrentados na terapia destas doenças têm sido usados análogos de nucleótidos e/ou nucleósidos como agentes terapêuticos. Estes têm o propósito de inibir a síntese de novo dos nucleótidos em determinadas etapas, estando envolvidos na replicação e síntese do RNA e DNA nas células em divisão. Atuam por inibição específica de enzimas no metabolismo dos nucleótidos/nucleósidos ou ainda por incorporação no DNA ou no RNA. This study will be developed into two main subjects; one related to the use of compounds which interfere with the metabolism of purine- and pyrimidine- nucleotides as antineoplastic agents; another related to their use as antiviral agents. The nucleotides’ synthesis involves the construction of nucleic acids and the introduction of the nucleotides’ derivatives into other biochemical pathways and it is responsible for numerous functions of cellular metabolism. There are pathologies involving key enzymes from the nucleotides’ metabolism, which led to the synthesis of new drugs. Cancer is a disease that continues killing thousands of people, an effective and successful treatment has been a challenge. The same happens with some viral infections, mainly infections caused by HIV. To overcome the obstacles faced in the therapy of these diseases it has been used nucleotide and/or nucleoside analogues as therapeutic agents. These agents have the purpose of inhibiting the de novo nucleotide synthesis in certain steps, by being involved in RNA and DNA replication and synthesis in dividing cells. They act by specific enzymes inhibition in nucleotide/nucleoside metabolism and by incorporation into DNA or RNA.
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Wei, Shuang. "Modifications du metabolisme des nucleotides en relation avec la differenciation et en reponse a une irradiation dans des cellules tumorales humaines (doctorat : structure et fontionnement des systemes biologiques integres)." Paris 11, 1998. http://www.theses.fr/1998PA114846.

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Books on the topic "Purine nucleotides"

1

Pharmacology of purine and pyrimidine receptors. San Diego, CA: Elsevier, 2011.

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M, Poltavchenko G., ed. Rolʹ adenozina v reguli͡a︡t͡s︡ii fiziologicheskikh funkt͡s︡iĭ organizma. Sankt-Peterburg: "Nauka," S.-Peterburgskoe otd-nie, 1991.

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Wilkinson, Yvonne Annette. Nucleotide pool changes resulting from purine and pyrimidine salrage pathway deficiency in Friend erythroleukaemia cells. [s.l: The Author], 1989.

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Amara, Francis Morigua. The significance of purine salvage pathway enzymes in mutagenesis and nucleotide metabolism in friend erythroleukaemia cells. [s.l: The Author], 1990.

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1953-, Jacobson Kenneth Alan, and Jarvis Michael F, eds. Purinergic approaches in experimental therapeutics. New York: Wiley-Liss, 1997.

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1951-, Lusty James R., Wearden Peter, and Moreno Virtudes, eds. CRC handbook of nucleobase complexes: Transition metal complexes of naturally occuring nucleobases and their derivatives. Boca Raton, Fla: CRC Press, 1990.

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Zhao, Xiaoqin S. Purine nucleotide-induced seizures in rat prepiriform cortex. 1994.

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Zhao, Xiaoqin S. Purine nucleotide-induced seizures in rat prepiriform cortex. 1994.

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Weisman, Gary A., Jeffrey S. Fedan, and John T. Turner. P2 Nucleotide Receptors. Humana Press, 2012.

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Professor, Turner John T., Weisman Gary A, and Fedan Jeffrey S, eds. The P2 nucleotide receptors. Totowa, N.J: Humana Press, 1998.

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Book chapters on the topic "Purine nucleotides"

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Srivastava, Prem C., Roland K. Robins, and Rich B. Meyer. "Synthesis and Properties of Purine Nucleosides and Nucleotides." In Chemistry of Nucleosides and Nucleotides, 113–281. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-0995-6_2.

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Achterberg, P. W. "Adenine Nucleotides, Purine Metabolism and Myocardial Function." In Developments in Cardiovascular Medicine, 45–52. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1319-6_5.

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Rudolph, Frederick B., William C. Fanslow, Anil D. Kulkarni, Sulabha S. Kulkarni, and Charles T. Van Buren. "Effect of Dietary Nucleotides on Lymphocyte Maturation." In Purine and Pyrimidine Metabolism in Man V, 497–501. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5104-7_83.

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Havel, Michael, Werner Monl, Gerhard Schopf, and Mathias M. Müller. "Purine Nucleotides in Human Hearts During Open Heart Surgery." In Purine and Pyrimidine Metabolism in Man V, 529–33. New York, NY: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-1248-2_82.

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Nuki, G., K. Astrini, D. Brenton, M. Cruikshank, J. Lever, and J. E. Seegmiller. "Purine and Pyrimidine Nucleotides in Some Mutant Human Lymphoblasts." In Ciba Foundation Symposium 48 - Purine and Pyrimidine Metabolism, 127–42. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720301.ch9.

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Peters, Godefridus J. "Therapy Related Disturbances in Nucleotides in Cancer Cells." In Purine and Pyrimidine Metabolism in Man VIII, 95–107. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-2584-4_24.

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Danchin, Antoine. "Are Purine Nucleoside Triphosphate Cyclases an Example of Convergent Evolution?" In Adenine Nucleotides in Cellular Energy Transfer and Signal Transduction, 365–77. Basel: Birkhäuser Basel, 1992. http://dx.doi.org/10.1007/978-3-0348-7315-4_33.

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Nakabeppu, Yusaku, Mehrdad Behmanesh, Hiroo Yamaguchi, Daisuke Yoshimura, and Kunihiko Sakumi. "Prevention of the Mutagenicity and Cytotoxicity of Oxidized Purine Nucleotides." In Oxidative Damage to Nucleic Acids, 40–53. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-72974-9_3.

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Pankiewicz, Krzysztof W., and Kyoichi A. Watanabe. "A Synthesis of 2’-Fluoro- and 3’-Fluoro-Substituted Purine Nucleosides via a Direct Approach." In Nucleosides and Nucleotides as Antitumor and Antiviral Agents, 55–71. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2824-1_3.

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Edwards, N. Lawrence, Annette M. Zaytoun, and Gail A. Renard. "Separate Mechanisms for Cellular uptake of Purine Nucleotides by B- and T-Lymphoblasts." In Purine and Pyrimidine Metabolism in Man V, 463–65. New York, NY: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-1248-2_72.

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Conference papers on the topic "Purine nucleotides"

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Matsuyama, Masahiro, Masatoshi Wakui, Makoto Monnai, Tomoko Mizushima, Chiyoko NIshime, Kenji Kawai, Hiroshi Suemizu, et al. "Abstract 2366: Reduced ecto-5′-nucleotidase CD73 expression and altered purine nucleotide metabolism in colorectal cancer cells robustly causing liver metastases." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2366.

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Khancheuski, M. А., V. N. Lesik, and E. I. Kvasyuk. "SYNTHESIS OF 8-BROMOADENOSINE AT DIFFERENT PH VALUES." In SAKHAROV READINGS 2021: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute of Belarusian State University, 2021. http://dx.doi.org/10.46646/sakh-2021-2-132-135.

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This article shows methods for the preparation of 8-bromoadenosine which is an important intermediate in the syntheses of analogs of purines nucleosides and nucleotides with a broad spectrum of biological activity. The influence of the pH values of the medium on the yield of 8-bromoadenosine was studied. It was showed that pH 4.3 is optimal for the preparation of 8-bromoadenosine by reaction of adenosine with a solution of bromine in water.
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Česnek, Michal, Michal Hocek, and Antonín Holý. "Cross-coupling reactions of 2-amino-6-halopurine derivatives with organometallic reagents leading to 6-alkylated purine acyclic nucleotide analogues." In XIth Symposium on Chemistry of Nucleic Acid Components. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 1999. http://dx.doi.org/10.1135/css199902255.

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Al-Husseiny, Istabraq A., Maysaa K. Al-Malkey, Ibtesam B. Hassan, Ali A. Rabaan, Samer S. Kadhim, and Alaudeen S. Khlaf. "Interleukin 2−330 single nucleotide polymorphism association with type 1 diabetes in Iraqi patients." In PROCEEDING OF THE 1ST INTERNATIONAL CONFERENCE ON ADVANCED RESEARCH IN PURE AND APPLIED SCIENCE (ICARPAS2021): Third Annual Conference of Al-Muthanna University/College of Science. AIP Publishing, 2022. http://dx.doi.org/10.1063/5.0093594.

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Mitchell-Ryan, Shermaine K., Lei Wang, Steven Orr, Sita Kugel, Christina Cherian, Aleem Gangjee, and Larry H. Matherly. "Abstract 5494: Novel 6-substituted pyrrolo[2,3-d]pyrimidine thienoyl antifolate regioisomers target folate receptor alpha positive ovarian cancer cells via inhibition of de novo purine nucleotide biosynthesis." In 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.am2013-5494.

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Wallace-Povirk, Adrianne, Nian Tong, Carrie O'Connor, Zhanjun Hou, Aleem Gangjee, Larry Matherly, and Xilin Zhou. "Abstract 3983: Tumor-targeting with novel dual-targeted 6-substituted thieno[2,3-d]pyrimidine antifolates via cellular uptake by folate receptor α, and inhibition of de novo purine nucleotide biosynthesis." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3983.

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Lavén, Gaston, and Jacek Stawinski. "A new synthetic route to diastereomerically pure P-chiral nucleotide analogues, dinucleoside benzylphosphonates, via stereospecific Pd(0) catalyzed cross-coupling reaction." In XIVth Symposium on Chemistry of Nucleic Acid Components. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2008. http://dx.doi.org/10.1135/css200810395.

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Reports on the topic "Purine nucleotides"

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Levisohn, Sharon, Maricarmen Garcia, David Yogev, and Stanley Kleven. Targeted Molecular Typing of Pathogenic Avian Mycoplasmas. United States Department of Agriculture, January 2006. http://dx.doi.org/10.32747/2006.7695853.bard.

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Intraspecies identification (DNA "fingerprinting") of pathogenic avian mycoplasmas is a powerful tool for epidemiological studies and monitoring strain identity. However the only widely method available for Mycoplasma gallisepticum (MG) and M. synoviae (MS)wasrandom amplified polymorphic DNA (RAPD). This project aimed to develop alternative and supplementary typing methods that will overcome the major constraints of RAPD, such as the need for isolation of the organism in pure culture and the lack of reproducibility intrinsic in the method. Our strategy focussed on recognition of molecular markers enabling identification of MG and MS vaccine strains and, by extension, pathogenic potential of field isolates. Our first aim was to develop PCR-based systems which will allow amplification of specific targeted genes directly from clinical material. For this purpose we evaluated the degree of intraspecies heterogeneity in genes encoding variable surface antigens uniquely found in MG all of which are putative pathogenicity factors. Phylogenic analysis of targeted sequences of selected genes (pvpA, gapA, mgc2, and lp) was employed to determine the relationship among MG strains.. This method, designated gene targeted sequencing (GTS), was successfully employed to identify strains and to establish epidemiologically-linked strain clusters. Diagnostic PCR tests were designed and validated for each of the target genes, allowing amplification of specific nucleotide sequences from clinical samples. An mgc2-PCR-RFLP test was designed for rapid differential diagnosis of MG vaccine strains in Israel. Addressing other project goals, we used transposon mutagenesis and in vivo and in vitro models for pathogenicity to correlated specific changes in target genes with biological properties that may impact the course of infection. An innovative method for specific detection and typing of MS strains was based on the hemagglutinin-encoding gene vlhA, uniquely found in this species. In parallel, we evaluated the application of amplified fragment length polymorphism (AFLP) in avian mycoplasmas. AFLP is a highly discriminatory method that scans the entire genome using infrequent restriction site PCR. As a first step the method was found to be highly correlated with other DNA typing methods for MG species and strain differentiation. The method is highly reproducible and relatively rapid, although it is necessary to isolate the strain to be tested. Both AFLP and GTS are readily to amenable to computer-assisted analysis of similarity and construction of a data-base resource. The availability of improved and diverse tools will help realize the full potential of molecular typing of avian mycoplasmas as an integral and essential part of mycoplasma control programs.
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