Hypoxanthine Phosphoribosyltransferase
Mostrando 13-24 de 285 artigos, teses e dissertações.
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13. Effect of 6-thioguanine on Chlamydia trachomatis growth in wild-type and hypoxanthine-guanine phosphoribosyltransferase-deficient cells.
Chlamydiae have evolved a biphasic life cycle to facilitate their survival in two discontinuous habitats. The unique growth cycle is represented by two alternating forms of the organism, the elementary body and the reticulate body. Chlamydiae have an absolute nutritional dependency on the host cell to provide ribonucleoside triphosphates and other essential
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14. Proposed explanation for S-adenosylhomocysteine hydrolase deficiency in purine nucleoside phosphorylase and hypoxanthine-guanine phosphoribosyltransferase-deficient patients.
We have examined the basis for the recently reported, but unexplained deficiency of S-adenosylhomocysteine hydrolase (AdoHcyase) in the erythrocytes of patients with genetic deficiencies of purine nucleoside phosphorylase and hypoxanthine-guanine phosphoribosyltransferase. We found that a hemolysate from a patient with purine nucleoside phosphorylase deficie
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15. 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
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16. 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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17. Nature of 6-methylpurine inhibition and characterization of two 6-methylpurine-resistant mutants of Neurospora crassa.
6-Methylpurine, an analog of adenine, inhibits the growth of Neurospora crassa. From kinetic studies it was found that 6-methylpurine is converted to its nucleotide form by adenine phosphoribosyltransferase (EC 2.4.2.7), and inhibits the de novo purine biosynthesis. Adenine relieves the growth inhibition caused by 6-methylpurine, whereas hypoxanthine is not
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18. Hypoxanthine phosphoribosyltransferase deficiency: association of reduced catalytic activity with reduced levels of immunologically detectable enzyme protein.
In the present study hemolysates from fourteen patients with a genetically determined deficiency of hypoxanthine phosphoribosyltransferase (EC 2.4.2.8; IMP:pyrophosphate phosphoribosyltransferase) activity were examined immunologically for the presence of material that crossreacts with the normal enzyme. A quantitative assay for crossreacting material in enz
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19. Serial transfer of a human gene to rodent cells by sequential chromosome-mediated gene transfer.
The human hypoxanthine phosphoribosyl-transferase (IMP:pyrophosphate phosphoribosyltransferase, EC 2.4.2.8) gene (hprt) has been serially transferred to mouse cells and then to Chinese hamster fibroblasts by two cycles of metaphase chromosome isolation and incubation with recipient cells. Human metaphase chromosomes were incubated with mouse A9 cells deficie
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20. Isolation of mammalian cell mutants deficient in glucose-6-phosphate dehydrogenase activity: linkage to hypoxanthine phosphoribosyl transferase.
Mutants of Chinese hamster ovary cells deficient in glucose-6-phosphate dehydrogenase (D-glucose-6-phosphate: NADP 1-oxidoreducatse, EC 1.1.1.49) activity were isolated after mutagenesis with ethyl methane sulfonate. The mutants were induced at frequencies of about 10-4 and do not differ in growth properties from wild-type cells. They were isolated by means
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21. Purine metabolism in cultured human fibroblasts derived from patients deficient in hypoxanthine phosphoribosyltransferase, purine nucleoside phosphorylase, or adenosine deaminase.
Rates of purine synthesis de novo, as measured by the incorporation of [14C]formate into newly synthesized purines, have been determined in cultured human fibroblasts derived from normal individuals and from patients deficient in adenosine deaminase, purine nucleoside phosphorylase, or hypoxanthine phosphoribosyltransferase, three consecutive enzymes of the
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22. Expression of the Methanobacterium thermoautotrophicum hpt Gene, Encoding Hypoxanthine (Guanine) Phosphoribosyltransferase, in Escherichia coli
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 s
American Society for Microbiology.
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23. Germ-line transmission of a planned alteration made in a hypoxanthine phosphoribosyltransferase gene by homologous recombination in embryonic stem cells.
Embryonic stem cells (derived from 129/Ola mice) containing a mutant hypoxanthine phosphoribosyltransferase gene that had been corrected in vitro in a planned manner by homologous recombination were injected into blastocysts obtained from C57BL/6J mice. The injected blastocysts were introduced into pseudopregnant female mice to complete their development. El
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24. Evidence for DNA modification in the maintenance of X-chromosome inactivation of adult mouse tissues.
The role of DNA modification in the maintenance of mammalian X-chromosome inactivation was investigated by using the technique of DNA transformation in mammalian cells. The ability of inactive X-chromosome DNA from adult mouse tissues to act in transformation for the X-linked hypoxanthine phosphoribosyltransferase gene (Hprt) could be ascertained by utilizin