Adenine Phosphoribosyltransferase
Mostrando 13-24 de 127 artigos, teses e dissertações.
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13. Purine salvage pathways of Bacillus subtilis and effect of guanine on growth of GMP reductase mutants.
We have isolated numerous mutants containing mutations in the salvage pathways of purine synthesis. The mutations cause deficiencies in adenine phosphoribosyltransferase (adeF), in hypoxanthine-guanine phosphoribosyltransferase (guaF), in adenine deaminase (adeC), in inosine-guanosine phosphorylase, (guaP), and in GMP reductase (guaC). The physiological prop
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14. Genetic and physiological characterization of Bacillus subtilis mutants resistant to purine analogs.
Bacillus subtilis mutants defective in purine metabolism have been isolated by selecting for resistance to purine analogs. Mutants resistant to 2-fluoroadenine were found to be defective in adenine phosphoribosyltransferase (apt) activity and slightly impaired in adenine uptake. By making use of apt mutants and mutants defective in adenosine phosphorylase ac
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15. Adenine transport and binding in cultured mammalian cells deficient in adenine phosphoribosyltransferase.
Rapid kinetic techniques were employed to measure the transport of adenine in adenine phosphoribosyltransferase-deficient L929 and Chinese hamster ovary (CHO) cells in zero-trans entry and exit and equilibrium exchange procedures. The kinetic parameters of transport were computed by fitting appropriate integrated rate equations to time courses of transmembra
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16. Transcriptional activation of the adenine phosphoribosyltransferase promoter by an upstream butyrate-induced Moloney murine sarcoma virus enhancer-promoter element.
It has been documented that the activity of a specific promoter can be occluded by the presence of another promoter element upstream. We present evidence for a phenomenon contradictory to that predicted by the promoter occlusion theory. Transcription from the hamster aprt (adenine phosphoribosyltransferase) promoter was augmented instead of repressed in tran
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17. Induction of adenine salvage in mouse cell lines deficient in adenine phosphoribosyltransferase.
Adenine phosphoribosyltransferase (APRT) (EC 2.4.2.7) pseudorevertant cell lines were isolated under selective conditions requiring adenine salvage for survival; yet they were found to be deficient in measurable APRT activity and resistant to the purine analog 2'6'-diaminopurine (DAP) (M.S. Turker, J. A. Tischfield, P. Rabinovitch, P.J. Stambrook, J.J. Trill
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18. Diaminopurine-Resistant Mutants of Cultured, Diploid Human Fibroblasts
Clones of cells resistant to 2,6-diaminopurine were detected in skin fibroblast cultures derived from 13 of 21 normal humans of both sexes from 17 unrelated families. Almost all of the cultures that yielded mutants were chosen for further study from among a total of 83 surveyed because they displayed a slight resistance to low concentrations of diaminopurine
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19. Identification of a common nonsense mutation in Japanese patients with type I adenine phosphoribosyltransferase deficiency.
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20. Adenine phosphoribosyltransferase deficiency: a previously undescribed genetic defect in man
A deficiency of adenine phosphoribosyltransferase (A-PRTase) is described in four members in three generations of one family. A-PRTase is coded by an autosome and the mutants described in this report are heterozygotes for this enzyme defect. The level of enzyme activity in these heterozygotes was inappropriately low, ranging from 21 to 37% of normal rather t
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21. Purine-resistant Drosophila melanogaster result from mutations in the adenine phosphoribosyltransferase structural gene.
Mutants of Drosophila melanogaster selected for resistance to purine killing are deficient in adenine phosphoribosyltransferase (APRT; E.C. 2.4.2.7) activity. Genetic mapping and complementation analysis demonstrate that purine resistance, deficiency of APRT activity, and differences in the isoelectric point of APRT result from alterations at a single locus,
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22. Overproduction of Uric Acid in Hypoxanthine-Guanine Phosphoribosyltransferase Deficiency: CONTRIBUTION BY IMPAIRED PURINE SALVAGE
The contribution of reduced purine salvage to the hyperuricemia associated with hypoxanthine-guanine phosphoribosyltransferase deficiency was measured by the intravenous administration of tracer doses of [8-14C]adenine to nine patients with normal enzyme activity, three patients with a partial deficiency of hypoxanthine-guanine phosphoribosyltransferase, and
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23. Use of Escherichia coli Mutants to Evaluate Purines, Purine Nucleosides, and Analogues
Of 142 purines, purine nucleosides, and analogues tested for inhibition of growth of Escherichia coli B Hill, 45 were active. Of these, 27 were evaluated for inhibition of other E. coli lines, including those resistant to 6-thioguanine, 2-fluoroadenosine, 2,6-diaminopurine, or 6-mercaptopurine. Most toxic to the parent lines were 2-fluoroadenosine, 2-fluoroa
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24. Human gene expression in rodent cells after uptake of isolated metaphase chromosomes.
Permanent transfer of genetic information from chromosomes isolated from human diploid cells to recipient cells has been demonstrated. Human metaphase chromosomes were incubated with mouse A9 fibroblasts deficient in hypoxanthine phosphoribosyltransferase (IMP:pyrophosphate phosphoribosyltransferase, EC 2.4.2.8) and adenine phosphoribosyltransferase (AMP:pyr