Gotowe bibliografie tematyczne / Phosphoribosyltransferase

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Gotowa bibliografia na temat „Phosphoribosyltransferase”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 4 lutego 2022

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Artykuły w czasopismach na temat "Phosphoribosyltransferase"

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Fateev, Ilja V., Ekaterina V. Sinitsina, Aiguzel U. Bikanasova, Maria A. Kostromina, Elena S. Tuzova, Larisa V. Esipova, Tatiana I. Muravyova, Alexei L. Kayushin, Irina D. Konstantinova i Roman S. Esipov. "Thermophilic phosphoribosyltransferases Thermus thermophilus HB27 in nucleotide synthesis". Beilstein Journal of Organic Chemistry 14 (21.12.2018): 3098–105. http://dx.doi.org/10.3762/bjoc.14.289.

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Phosphoribosyltransferases are the tools that allow the synthesis of nucleotide analogues using multi-enzymatic cascades. The recombinant adenine phosphoribosyltransferase (TthAPRT) and hypoxanthine phosphoribosyltransferase (TthHPRT) from Thermus thermophilus HB27 were expressed in E.coli strains and purified by chromatographic methods with yields of 10–13 mg per liter of culture. The activity dependence of TthAPRT and TthHPRT on different factors was investigated along with the substrate specificity towards different heterocyclic bases. The kinetic parameters for TthHPRT with natural substrates were determined. Two nucleotides were synthesized: 9-(β-D-ribofuranosyl)-2-chloroadenine 5'-monophosphate (2-Сl-AMP) using TthAPRT and 1-(β-D-ribofuranosyl)pyrazolo[3,4-d]pyrimidine-4-one 5'-monophosphate (Allop-MP) using TthНPRT.
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Aklujkar, Muktak. "Two ATP phosphoribosyltransferase isozymes of Geobacter sulfurreducens contribute to growth in the presence or absence of histidine and under nitrogen fixation conditions". Canadian Journal of Microbiology 57, nr 7 (lipiec 2011): 547–58. http://dx.doi.org/10.1139/w11-047.

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Bacteria of the Geobacter clade possess two distinct ATP phosphoribosyltransferases encoded by hisGL and hisGS+hisZ to catalyze the first reaction of histidine biosynthesis. This very unusual redundancy was investigated by mutational analysis. The hisGL, hisGS, and hisZ genes of Geobacter sulfurreducens were deleted, effects on growth and histidine biosynthesis gene expression were evaluated, and deficiencies were complemented with plasmid-borne genes. Both hisGL and hisGS+hisZ encode functional ATP phosphoribosyltransferases. However, deletion of hisGL resulted in no growth defect, whereas deletion of hisGS delayed growth when histidine was not provided. Both deletions increased hisZ transcript abundance, and both ΔhisGS and ΔhisZ mutations increased hisGL transcript abundance. Growth with HisGL alone (due to deletion of either hisGS or hisZ) was better under nitrogen fixation conditions than when ammonium was provided. Deletion of hisZ caused growth defects under all conditions tested, with or without exogenous sources of histidine, with different patterns of histidine biosynthesis gene expression under each condition. Taken together, the data indicate that G. sulfurreducens depends primarily on the HisGSZ isozyme as an ATP phosphoribosyltransferase in histidine biosynthesis, and for other functions when histidine is available; however, HisGL also functions as ATP phosphoribosyltransferase, particularly during nitrogen fixation.
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Sauer, Jørgen, i Per Nygaard. "Expression of the Methanobacterium thermoautotrophicum hpt Gene, Encoding Hypoxanthine (Guanine) Phosphoribosyltransferase, in Escherichia coli". Journal of Bacteriology 181, nr 6 (15.03.1999): 1958–62. http://dx.doi.org/10.1128/jb.181.6.1958-1962.1999.

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ABSTRACT The hpt gene from the archaeon Methanobacterium thermoautotrophicum, encoding hypoxanthine (guanine) phosphoribosyltransferase, was cloned by functional complementation into Escherichia coli. The hpt-encoded amino acid sequence is most similar to adenine phosphoribosyltransferases, but the encoded enzyme has activity only with hypoxanthine and guanine. The synthesis of the recombinant enzyme is apparently limited by the presence of the rare arginine codons AGA and AGG and the rare isoleucine AUA codon on the hpt gene. The recombinant enzyme was purified to apparent homogeneity.
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Bollée, Guillaume, Jérôme Harambat, Albert Bensman, Bertrand Knebelmann, Michel Daudon i Irène Ceballos-Picot. "Adenine Phosphoribosyltransferase Deficiency". Clinical Journal of the American Society of Nephrology 7, nr 9 (14.06.2012): 1521–27. http://dx.doi.org/10.2215/cjn.02320312.

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Kadziola, A., K. S. Jensen, A. Mølgaard, J. C. N. Poulsen i K. F. Jensen. "Sulfolobus solfataricusadenine phosphoribosyltransferase". Acta Crystallographica Section A Foundations of Crystallography 67, a1 (22.08.2011): C786—C787. http://dx.doi.org/10.1107/s0108767311080093.

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Munagala, Narsimha, Anne E. Sarver i Ching C. Wang. "Converting the Guanine Phosphoribosyltransferase fromGiardia lambliato a Hypoxanthine-guanine Phosphoribosyltransferase". Journal of Biological Chemistry 275, nr 47 (6.09.2000): 37072–77. http://dx.doi.org/10.1074/jbc.m007239200.

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OLIVEIRA, DENILSON F., HELVÉCIO M. DOS SANTOS JÚNIOR, ALEXANDRO S. NUNES, VICENTE P. CAMPOS, RENATA S. C. DE PINHO i GIOVANNA C. GAJO. "Purification and identification of metabolites produced by Bacillus cereus and B. subtilis active against Meloidogyne exigua, and their in silico interaction with a putative phosphoribosyltransferase fromM. incognita". Anais da Academia Brasileira de Ciências 86, nr 2 (czerwiec 2014): 525–38. http://dx.doi.org/10.1590/0001-3765201402412.

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To contribute to the development of products to controlMeloidogyne exigua, the bacteria Bacillus cereus and B. subtilis were cultivated in liquid medium to produce metabolites active against this plant-parasitic nematode. Fractionation of the crude dichloromethane extracts obtained from the cultures afforded uracil, 9H-purine and dihydrouracil. All compounds were active against M. exigua, the latter being the most efficient. This substance presented a LC50 of 204 µg/mL against the nematode, while a LC50 of 260 µg/mL was observed for the commercial nematicide carbofuran. A search for protein-ligand complexes in which the ligands were structurally similar to dihydrouracil resulted in the selection of phosphoribosyltransferases, the sequences of which were used in an in silico search in the genome of M. incognita for a similar sequence of amino acids. The resulting sequence was modelled and dihydrouracil and 9H-purine were inserted in the active site of this putative phosphoribosyltransferase resulting in protein-ligand complexes that underwent molecular dynamics simulations. Calculation of the binding free-energies of these complexes revealed that the dissociation constant of dihydrouracil and 9H-purine to this protein is around 8.3 x 10-7 and 1.6 x 10-6 M, respectively. Consequently, these substances and the putative phosphoribosyltransferase are promising for the development of new products to control M. exigua.
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Jardim, Armando, Susan E. Bergeson, Sarah Shih, Nicola Carter, Randall W. Lucas, Gilles Merlin, Peter J. Myler, Kenneth Stuart i Buddy Ullman. "Xanthine Phosphoribosyltransferase fromLeishmania donovani". Journal of Biological Chemistry 274, nr 48 (26.11.1999): 34403–10. http://dx.doi.org/10.1074/jbc.274.48.34403.

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Pittelli, Maria, Laura Formentini, Giuseppe Faraco, Andrea Lapucci, Elena Rapizzi, Francesca Cialdai, Giovanni Romano, Gloriano Moneti, Flavio Moroni i Alberto Chiarugi. "Inhibition of Nicotinamide Phosphoribosyltransferase". Journal of Biological Chemistry 285, nr 44 (19.08.2010): 34106–14. http://dx.doi.org/10.1074/jbc.m110.136739.

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OLESEN, UFFE HØGH, NINA HASTRUP i MAXWELL SEHESTED. "Expression patterns of nicotinamide phosphoribosyltransferase and nicotinic acid phosphoribosyltransferase in human malignant lymphomas". APMIS 119, nr 4-5 (25.03.2011): 296–303. http://dx.doi.org/10.1111/j.1600-0463.2011.02733.x.

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Rozprawy doktorskie na temat "Phosphoribosyltransferase"

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Catton, Gemma R. "Mechanistic studies on quinolinate phosphoribosyltransferase /". St Andrews, 2007. http://hdl.handle.net/10023/485.

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Catton, Gemma Rachel. "Mechanistic studies on quinolinate phosphoribosyltransferase". Thesis, University of St Andrews, 2008. http://hdl.handle.net/10023/485.

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Quinolinate phosphoribosyltransferase (QPRTase, EC 2.4.2.19) is an intriguing enzyme which appears to catalyse two distinct chemical reactions; transfer of a phosphoribosyl moiety from 5-phosphoribosyl-1-pyrophosphate to the nitrogen of quinolinic acid and decarboxylation at the 2-position to give nicotinic acid mononucleotide. The chemical mechanism of QPRTase is not fully understood. In particular, enzymatic involvement in the decarboxylation step is yet to be conclusively proven. QPRTase is neurologically important as it degrades the potent neurotoxin, quinolinic acid, implicated in diseases such as Huntington’s disease and AIDS related dementia. Due to its neurological importance and unusual chemistry the mechanism of QPRTase is important. Described here is a mechanistic study on human brain QPRTase. Human brain QPRTase was successfully expressed in E. coli BL21 (DE3) from the pEHISTEV-QPRTase construct and the protein was efficiently purified by nickel affinity chromatography. The crystal structure was solved using multiwavelength methods to a resolution of 1.9 Å. Human brain QPRTase was found to adopt an energetically stable hexameric arrangement. The enzyme was also found to exist as a hexamer during gel filtration under physiological conditions. Kinetic studies allowed the measurement of the kinetic parameters for quinolinic acid. The data gave a Km of 13.4 ± 1.0 μM and a Vmax of 0.92 ± 0.01 μM min-1. There was no evidence for cooperative binding of quinolinic acid to the six subunits of the QPRTase hexamer. The enzyme showed maximum activity at approximately pH 6. The active site of human brain QPRTase is a deep pocket with a highly positive electrostatic surface composed of three arginine residues, two lysine residues and one histidine residue. Mutation of these residues resulted in either complete loss or significant reduction in enzymatic activity showing they are important for binding and/or catalysis. A possible mechanism involving QPRTase in the decarboxylation of quinolinic acid mononucleotide was proposed. A series of quinolinic acid analogues were synthesised and tested as inhibitors of QPRTase. The inhibition studies highlighted some key interactions in the active site.
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Marinaki, Anthony Marin. "The biochemical and molecular basis of Hypoxanthine-guanine phosphoribosyltransferase deficiency". Doctoral thesis, University of Cape Town, 1996. http://hdl.handle.net/11427/26969.

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Hypoxanthine-guanine phosphoribosyltransferase (HPRT) catalyses the first step in purine salvage. A complete deficiency of the enzyme results in the devastating neurological symptoms of the Lesch-Nyhan syndrome. The Lesch-Nyhan syndrome is characterised by purine overproduction leading to, hyperuricemia and gout and a central nervous system disorder characterised by severe, spasticity, choreoathetosis, mental retardation and compulsive self-mutilatory behaviour, A partial deficiency of the enzyme results in purine overproduction, gout and occasionally, mild neurological symptoms. Patients are spared the compulsive self-mutilation of the Lesch-Nyhan syndrome. The major part of the thesis consists of the characterisation of the molecular defects in nine patients with the Lesch-Nyhan syndrome. The polymerase chain reaction was used to amplify reverse transcribed HPRT mRNA. The coding region of the amplified HPRT cDNA was either directly sequenced, or cloned and sequenced. All the mutations characterised were insertion or deletion events which resulted in premature termination of the predicted protein. Three patients were found to have a deletion of exon 7, two patients had single base insertions, while two patients appeared to have a complete deletion of the HPRT gene. An insertion in one patient was the result of a mutation within. intron 6 which created a new splice donor site. The new splice donor site in concert with a cryptic splice acceptor resulted in the creation of a new exon. A deletion of exons 2, 3 and 4 in another patient was found to lead to the alternative splicing of exon 5. These unusual splice junction mutations provided in viva support for the exon definition model of pre-mRNA splicing.
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Murungi, Edwin Kimathi. "Purification and characterisation of plasmodium falciparum Hypoxanthine phosphoribosyltransferase". Thesis, University of the Western Cape, 2007. http://etd.uwc.ac.za/index.php?module=etd&action=viewtitle&id=gen8Srv25Nme4_9199_1257245819.

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Malaria remains the most important parasitic disease worldwide. It is estimated that over 500 million infections and more that 2.7 million deaths arising from malaria occur each year. Most (90%) of the infections occur in Africa with the most affected groups being children of less than five years of age and women. this dire situation is exacerbated by the emrggence of drug resistant strains of Plasmodium falciparum. The work reported in this thesis focuses on improving the purification of PfHPRT by investigating the characteristics of anion exchange DE-52 chromatography (the first stage of purification), developing an HPLC gel filtration method for examining the quaternary structure of the protein and possible end stage purification, and initialcrystalization trials. a homology model of the open, unligaded PfHPRT is constructed using the atoomic structures of human, T.ccruz and STryphimurium HPRT as templates.

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Ford, Barry Noel. "Structure-function relationships in Chinese hamster adenine phosphoribosyltransferase". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ34263.pdf.

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Shahabuddin, Mohammed. "Molecular studies on the hypoxanthine phosphoribosyltransferase of Plasmodium falciparum". Thesis, University of Edinburgh, 1990. http://hdl.handle.net/1842/14382.

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Hypoxanthine phosphoribosyltransferase (EC 2.7.2.8) of P.falciparum has been studied for its biological properties and cellular location. The enzyme plays an important role in the parasite's life, and therefore is a putative target for chemotherapy against malaria. Due to the difficulty in obtaining large amounts of the enzyme from the parasite, it was over-expressed in E.coli, first as a fusion protein with E.co/i-j8-galactosidase. This facilitated the one step purification of the protein, using /3-galactosidase substrate affinity chromatography, for making antibodies against the enzyme. The antibodies thus made were used to investigate the cellular location, a prerequisite for a successful drug design against the parasite enzyme. Im-munofluorescent microscopy (IFA) and immunogold electron microscopy revealed that; 1. the enzyme is expressed at all the stages of the parasite's life, 2. the enzyme is concentrated in some vesicular bodies of unknown origin, 3. in the sporozoite, it may be released into the intrapellicular spaces. Subsequently, the enzyme was over-expressed directly in E.coli, as a non-fusion protein and retained its enzymatic activity. This opened the way to study the enzyme for its biochemical properties and structure-activity relationship. The active E.co/i-expressed P.falciparum HPRT compensated a S.typhimurium hpt mutation. The strain, named S.lyphimurium SH4 can now be used to screen large numbers of putative antimalarial drugs which might act against the parasite HPRT. This will be both simple and inexpensive. The cell free extract of induced SH4 was used to study some biochemical properties of the enzyme. Such a study confirmed the finding that unlike any other Plasmodia studied so far, P.falciparum HPRT can use xanthine as its substrate in addition to hypoxanlhine and guanine. However, competitive inhibition studies revealed that hypoxanthine is the most favourable substrate. The possible biological significance of such properties is discussed.
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Mittelstädt, Gerd Horst. "Allosteric regulation of the adenosine triphosphate phosphoribosyltransferase from campylobacter jejuni". Thesis, University of Canterbury. Chemistry, 2015. http://hdl.handle.net/10092/10799.

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The enzyme adenosine triphosphate phosphoribosyltransferase (ATP-PRT) catalyses the first reaction of the histidine biosynthetic pathway. ATP-PRT also represents a metabolic control point, directing the flux of metabolites through this energetically expensive pathway. Two distinctly different forms of ATP-PRT exist, the long form and the short form, which differ in the presence of a C-terminal regulatory domain. In the short form, where this domain is absent, it is functionally replaced by a regulatory protein, called HisZ. ATP-PRT activity is modulated by two layers of regulation: active site inhibition by adenosine monophosphate, which reflects cellular energy levels, and pathway end product feedback inhibition by histidine. In the long form ATP-PRT histidine binds to the allosteric site at the regulatory domain, but the exact nature of the inhibitory mechanism is still debated. This thesis characterises a new member of the ATP-PRT long form from Campylobacter jejuni (CjeATP-PRT) and investigates the molecular mechanisms involved in the feed back inhibition by histidine. Chapter 2 describes the characterisation of the CjeATP-PRT including a detailed description of its crystal structure. The C. jejuni enzyme is similar to the previously described enzymes of the ATP-PRT long form, but exists only as hexameric species under experimental conditions, which contradicts previous assumptions that the hexamer is exclusively inactive. Chapter 3 investigates the catalytic apparatus of CjeATP-PRT by separating the catalytic and regulatory domains of the enzyme for individual study. The isolated catalytic portion of the enzyme, the CjeATP-PRT Core mutant, forms a dimeric species with very limited catalytic capabilities but high substrate and product affnities. The CjeATP-PRT Core characteristics suggest that it exists in a permanently inhibited conformation, highlighting the requirement of the regulatory domain not only for feedback regulation but also for enzyme function. Additionally this supports the evolutionary need for the recruitment of a regulatory apparatus. In chapter 4 a potential intramolecular communication pathway from the allosteric to the active site is probed by the generation of several single site mutations. One of these, CjeATP-PRT R216A, is completely insensitive to histidine inhibition, although this ligand is still able to bind at the allosteric site, which is consistent with the involvement of R216 in the allosteric signal communication. The catalytic abilities of CjeATP-PRT R216A are largely impaired, leading to the assumption that this mutation causes a permanent inhibitory response. In summary this thesis supports the existence of a simple physical regulatorymechanism for the feedback inhibition of the ATP-PRT long form, the change between two different hexamer conformations depending on the presence of the allosteric effector.
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Evans, Laura. "Investigating the role of nicotinamide phosphoribosyltransferase (NAMPT) in cartilage catabolism". Thesis, Cardiff University, 2013. http://orca.cf.ac.uk/58335/.

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NAMPT (nicotinamide phosphoribosyltransferase) is a universally expressed protein elevated in the serum and synovial fluid of rheumatoid arthritis (RA) sufferers. NAMPT is a rate-limiting enzyme in the biosynthesis of (nicotinamide adenine dinucleotide) NAD+, an essential cellular coenzyme, and has also been shown to exert cytokine-like activities as a mediator of innate immunity. However little is currently known of the role of NAMPT in cartilage metabolism. In this thesis, the role and regulation of NAMPT was studied in a variety of model systems. Addition of exogenous (e)NAMPT to fibroblasts in vitro increased MMP-3 release, an effect attenuated by APO866. In vivo studies in a murine arthritis model showed APO866 treatment reduced arthritis index, with a slight reduction in synovial hyperplasia, inflammatory infiltrate and cartilage degradation. In vivo imaging with MMP activatable fluorescent probes showed a reduction in MMP activity in APO866-treated animals compared with placebo. Analyses of archived tissue indicated that APO866 reduced MMP gene expression in affected limbs in a time and dose dependent manner. In a cartilage explant culture system, APO866 significantly attenuated cytokine-mediated proteoglycan (PG) depletion and MMP-2 and -9 release. This was associated with a dose-dependent loss of cell viability. These effects were reversed by co-incubation with NAD+ metabolites NMN and NA, suggesting that cell survival was highly NAD+-dependent, and that cytokine-induced MMP expression could be NAMPT independent. Finally, in vitro studies in RA synovial fibroblasts revealed that intracellular (i)NAMPT is upregulated by cytokine stimulation, with concurrent upregulation of MMPs -1 and -3. The data emphasise the pleiotropic function of NAMPT in health and disease, and suggest a role for extracellular (but not intracellular) NAMPT in cartilage catabolism. Finally, NAMPT inhibition is highlighted as a promising therapeutic strategy for RA.
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Duckworth, Megan Jane Medical Sciences Faculty of Medicine UNSW. "Characterisation of the xanthineguanine phosphoribosyltransferase of helicobacter pylori as a potential therapeutic target". Publisher:University of New South Wales. Medical Sciences, 2008. http://handle.unsw.edu.au/1959.4/43418.

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Helicobacter pylori infects more than half of the global population and causes gastric disorders. The increasing development of antibiotic resistance by the bacterium continues to limit treatment options. The identification and characterisation of novel therapeutic targets are necessary for successful future treatment of the infection. One potential target for therapeutic intervention is the gpt gene encoded by hp0735 (jhp0672) in H. pylori strain 26695 (J99). This gene produces a putative xanthine-guanine phosphoribosyltransferase (XGPRTase), an enzyme of the purine salvage synthesis pathway. This project employed theoretical, molecular and biochemical approaches to investigate features of H. pylori gpt and XGPRTase that will serve to ascertain their therapeutic potential. The production of a functional XGPRTase by H. pylori was investigated in cell-free extracts, and the kinetic parameters of this activity were compared to those of purified rXGPRTase enzyme. The three 6-oxopurine substrates were recognised by rXGPRTase and allosteric kinetics were observed for some substrates of the enzyme in cell-free extracts and for purified enzyme. These observations indicate complex regulation and an influence of cellular interactions on activity. Bioinformatics were employed to analyse XGPRTase phylogeny, and threading techniques used to build a structural model of XGPRTase. The enzyme is significantly divergent from the equivalent mammalian enzyme, and modelling identified specific features of the enzyme. Molecular approaches were utilised to analyse the essential role of gpt in H. pylori survival. These included insertional inactivation of the gpt in wild-type H. pylori strains and in mutants possessing a complementing copy of the gene present at the rdxA locus. No mutants were recovered with inactivated gpt possibly as a result of pleiotropic effects. Plasmid-mediated complementation was attempted employing IPTG-inducible shuttle vectors and did not yield any mutants. Further characterisation of H. pylori XGPRTase was performed by determining the effects of nucleotide monophosphates and purine analogues on enzyme activity. Inhibition by GMP was observed in all cases, however differences in the inhibition by other nucleotide monophosphates were found between cell-free extracts and the recombinant enzyme. Inhibition of rXGPRTase activity was observed by the purine analogue 6-mercaptopurine ribose, a compound that previously has been shown to inhibit H. pylori growth in culture.
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Phehane, Vuyisile Ntosi. "The expression and drug targeting of parasitic hypoxanthine-guanine phosphoribosyltransferase (HGPRT)". Doctoral thesis, University of Cape Town, 2002. http://hdl.handle.net/11427/2701.

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Bibliography: leaves 231-243.
We have expressed and purified human, two forms of P. falciparum, and Toxoplasma gondii hypoxanthine-guanine phosphoribosyltransferase (HPRT) in E. coli using the pET expression system. The cDNA encoding the ORF of HPRT was amplified by PCR and transformed into E. coli cells using standard methods. Expression was induced by IPTG and reached about 13% of the total cell protein for all four proteins. The HPRTs were purified by nickel affinity chromatography most of the expressed protein could be isolated from the crude supernatant fraction in a soluble form. Human HPRT was active, with activity levels in the region of 38 umoles GMP min⁻¹ mg⁻¹ at 37 ⁰C, which is comparable to published literature values.
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Książki na temat "Phosphoribosyltransferase"

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Nelson, Aileen A. The significance of adenine phosphoribosyltransferase for DNA excision repair processes in friend erythrdeukaemia cells. [S.l: The Author], 1996.

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Renwick, Pamela Jean. Inter-individual variation in the molecular genetic architecture of the hypoxanthine phosphoribosyltransferase encoding region of man. Birmingham: University of Birmingham, 1996.

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Ceballos-Picot, Irène, i H. A. Jinnah. Disorders of Purine Metabolism Affecting Adults. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0042.

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Defects in some of the enzymes of purine metabolism are known to be associated with specific clinical disorders that may manifest at any age. Some of these disorders first present in adulthood, while many present earlier but go undiagnosed until adulthood. This chapter describes the disorders for which the metabolic basis is well characterized, in particular Lesch-Nyhan disease caused by a deficiency of hypoxanthine-guanine phosphoribosyltransferase (HPRT) and characterized by hyperuricemia, and variable motor and cognitive disability. Adenine phosphoribosyltransferase (APRT) deficiency is a not well known disease, and sometimes the diagnosis is made only after renal insufficiency is irreversible in adult patients.
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Części książek na temat "Phosphoribosyltransferase"

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Haubeck, H. D. "Adenin-Phosphoribosyltransferase". W Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_94-1.

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Haubeck, H. D. "Adenin-Phosphoribosyltransferase". W Springer Reference Medizin, 25. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_94.

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Schomburg, Dietmar, i Dörte Stephan. "Adenine phosphoribosyltransferase". W Enzyme Handbook 12, 969–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61117-9_213.

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Schomburg, Dietmar, i Dörte Stephan. "Hypoxanthine phosphoribosyltransferase". W Enzyme Handbook 12, 977–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61117-9_214.

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Schomburg, Dietmar, i Dörte Stephan. "Uracil phosphoribosyltransferase". W Enzyme Handbook 12, 985–89. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61117-9_215.

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Schomburg, Dietmar, i Dörte Stephan. "Orotate phosphoribosyltransferase". W Enzyme Handbook 12, 991–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61117-9_216.

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Schomburg, Dietmar, i Dörte Stephan. "Nicotinate phosphoribosyltransferase". W Enzyme Handbook 12, 997–1001. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61117-9_217.

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Schomburg, Dietmar, i Dörte Stephan. "Nicotinamide phosphoribosyltransferase". W Enzyme Handbook 12, 1003–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61117-9_218.

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Schomburg, Dietmar, i Dörte Stephan. "ATP phosphoribosyltransferase". W Enzyme Handbook 12, 1023–27. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61117-9_222.

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Schomburg, Dietmar, i Dörte Stephan. "Anthranilate phosphoribosyltransferase". W Enzyme Handbook 12, 1029–33. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61117-9_223.

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Streszczenia konferencji na temat "Phosphoribosyltransferase"

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Travelli, Cristina, Sara Morlacchi, Antonio Caldarelli, Antonio Sica i Armando A. Genazzani. "Abstract 1871: Targeting nicotinamide phosphoribosyltransferase (NAMPT) in cancer therapy." 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.am2013-1871.

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Sivordova, L., J. Polyakova, Y. Akhverdyan, V. Kravtsov, N. Fofanova i B. Zavodovsky. "AB1326 Nicotinamide phosphoribosyltransferase may be new factors contributing to osteoarthritis". W Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.3064.

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Moreno-Vinasco, L., J. Messana, T. Mirzapoiazova, E. Chiang, M. Brown, P. Singleton, S. Sammani, J. Moitra i J. Garcia. "Intracellular PBEF-Nicotinamide Phosphoribosyltransferase (NamPT) Activity Is Protective in VILI." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5564.

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Grolla, Ambra, Simone Torretta, Angela Amoruso, Giuseppe Orsomando i Armando Genazzani. "Abstract 440: Nicotinamide phosphoribosyltransferase (NAMPT): a new cytokine in tumor progression". W Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-440.

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Gibson, Anna E., Arnulfo Mendoza, Lioubov Korotchkina, Olga Chernova i Christine M. Heske. "Abstract 5477: Targeting nicotinamide phosphoribosyltransferase (NAMPT) with OT-82 in Ewing sarcoma". W 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.am2018-5477.

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Akhverdyan, Y., B. Zavodovsky, J. Polyakova, L. Seewordova, I. Zborovskaya i T. Rogatkina. "AB0288 Laboratory markers of inflammation and serum nicotinamide phosphoribosyltransferase level in rheumatoid arthritis patients". W Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.1958.

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Hocková, Dana, Antonín Holý, Michal Česnek, Ondřej Baszczyňski, Tomáš Tichý, Marcela Krečmerová, Zlatko Janeba i in. "Acyclic nucleoside phosphonates as inhibitors of hypoxanthine-guanine-xanthine phosphoribosyltransferase: new anti-malarial chemotherapy leads". W XVth Symposium on Chemistry of Nucleic Acid Components. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2011. http://dx.doi.org/10.1135/css201112171.

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Baumgart, Joshua T., Christine Heske, Mindy I. Davis, Kelli Wilson, Xiaoha Zhang, Rajarshi Guha, Marc Ferrer, Arnulfo Mendoza, Craig J. Thomas i Lee J. Helman. "Abstract 1930: Evaluating the effect of PARP inhibitors in combination with nicotinamide phosphoribosyltransferase inhibitors in Ewing sarcoma". W Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1930.

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Okumura, Shunsuke, Takaaki Sasaki i Yoshinobu Ohsaki. "Abstract 1770: A role of nicotinamide phosphoribosyltransferase in growth of KRAS mutant non-small cell lung cancer". W Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1770.

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Okumura, Shunsuke, Yoshinori Minami, Satoshi Endoh, Takaaki Sasaki, Kazuhiro Satoh, Masahiro Kitada i Yoshinobu Ohsaki. "Abstract 964: Nicotinamide phosphoribosyltransferase (Nampt) regulates growth of non-small cell lung cancer cells with c-Met overexpression". W Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-964.

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Raporty organizacyjne na temat "Phosphoribosyltransferase"

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Sivordova, L. E., J. V. Polyakova, Y. R. Akhverdyan, E. V. Papichev i B. V. Zavodovsky. LEVEL OF NICOTINAMIDE PHOSPHORIBOSYLTRANSFERASE AS PATHOGENETIC FACTORS CONTRIBUTING TO OSTEOARTHRITIS PROGRESSION. Планета, 2018. http://dx.doi.org/10.18411/978-5-907109-24-7-2018-xxxv-247-251.

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Jett, J. Pre-thymic somatic mutation leads to high mutant frequency at hypoxanthine-guanine phosphoribosyltransferase gene. Office of Scientific and Technical Information (OSTI), grudzień 1994. http://dx.doi.org/10.2172/98640.

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Akhverdyan, Y. R., B. V. Zavodovsky, J. V. Polyakova, L. E. Seewordova i O. D. Korolik. COMPARISON OF THE CONCENTRATION OF NICOTINAMIDE-PHOSPHORIBOSYLTRANSFERASE IN THE SERUM OF HEALTHY SUBJECTS AND PATIENTS WITH RHEUMATOID ARTHRITIS. Планета, 2018. http://dx.doi.org/10.18411/978-5-907109-24-7-2018-xxxiv-46-48.

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