Results 161 to 170 of about 579 (178)
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Uptake of Hypoxanthine in Human Erythrocytes

1977
The concentration of oxypurines in the plasma is known to be rather low (10 – 40 μM) (6). Since the formation of purines is accomplished to a great extent by the liver (7, 8), a transport of purines by erythrocytes from liver to tissues with limited or no capacity of de novo purine synthesis has been postulated (1, 3).
G. Falkner, Mathias Müller
openaire   +3 more sources

Partial hypoxanthine–guanine phosphoribosyl transferase deficiency without elevated urinary hypoxanthine excretion

Molecular Genetics and Metabolism, 2007
Partial hypoxanthine-guanine phosphoribosyl transferase (HGPRT) deficiency, also known as the Kelley-Seegmiller syndrome, can give rise to a wide range of neurological symptoms, and renal insufficiency. Biochemically, it is characterized by high uric acid concentrations in blood, high uric acid and hypoxanthine excretion in urine, and decreased ...
O. P. van Diggelen   +5 more
openaire   +4 more sources

The Spectrum of Hypoxanthine-guanine Phosphoribosyltransferase Deficiency

QJM: An International Journal of Medicine, 1973
The spectrum of clinical manifestations of hypoxanthine-guanine phosphoribosyltransferase (HGPRTase) deficiency is presented by reference to eight patients from five kindred. These patients illustrate the range of associated neurological findings, together with the variety of presentation and complications due to the associated over-production of urate.
Emmerson, B. T., Thompson, L.
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Hypoxanthine transport in normal and hypoxanthine guanine phosphoribosyltransferase (HGPRT) deficient diploid human lymphoblasts

Experimental Cell Research, 1977
Abstract We have examined the possible relation between hypoxanthine guanine phosphoribosyltransferase (EC 2.4.2.7., HGPRT) activity and hypoxanthine transport in the normal human lymphoblast line MGL8 and two HGPRT- mutant lines derived from it. The mutant line MGL8A29 (L8A29) had considerable amounts of material cross-reacting immunologically to ...
J. Epstein, J.W. Littlefield
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Salvage of circulating hypoxanthine by tissues of the mouse

Canadian Journal of Biochemistry and Cell Biology, 1983
Hypoxanthine is an inefficient precursor of purine nucleotides in mouse tissues. In vitro, mouse erythrocytes salvage <10% of hypoxanthine (10 μM) added to whole blood in 30 min of incubation at 37 °C. In vivo, circulating hypoxanthine is rapidly degraded (>90% in 10 min) to allantoin and uric acid. All tissues examined (other than erythrocytes)
J D Moyer, J F Henderson
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Mouse models of hypoxanthine phosphoribosyltransferase deficiency

Journal of Inherited Metabolic Disease, 1992
SummaryLesch‐Nyhan syndrome is an X‐linked disease caused by the deficiency of hypoxanthine phosphoribosyltransferase, an enzyme involved in the purine salvage pathways. It is characterized by severe gout, choreoathetosis, self‐mutilatory behaviour and mental retardation. The derivation of mice genetically deficient in this enzyme may help to elucidate
M. L. Hooper   +2 more
openaire   +3 more sources

Hypoxanthine–guanine phosphoribosyltransferase: further evidence for the identity of the binding sites for hypoxanthine and guanine

Canadian Journal of Biochemistry, 1969
Isotope exchange between hypoxanthine and both inosinate and guanylate, and between guanine and the same two ribonucleotides, support the view that hypoxanthine and guanine bind to the same site on hypoxanthine-guanine phosphoribosyltransferase.
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Synthesis of hypoxanthin from xanthin

Bulletin of the Academy of Sciences of the USSR Division of Chemical Science, 1969
We have described a preparative method for producing hypoxanthin by heating xanthin with a mixture of formamide and benzylamine.
S. I. Zav'yalov   +4 more
openaire   +2 more sources

Hypoxanthine and Xanthine Transport through the Blood-Brain Barrier in Hypoxanthine Phosphoribosyltransferase (HPRT) Deficiency

1989
Purine metabolism in the central nervous system (CNS) is characterized by: (i) reduced de novo purine synthesis (1), (ii) increased HPRT activity (2), and (iii) absence of detectable xanthine oxidase activity (3, 4). These facts determine that, instead of uric acid, the end products of purine nucleotide degradation in the CNS are hypoxanthine for ...
Juan G. Puig   +5 more
openaire   +3 more sources

Hypoxanthine Uptake by Isolated Brain Microvessels

1986
Brain is among the most active tissues in nucleotide and nucleic acid synthesis (1) but the role of the blood brain barrier in regulating the transport of purine and pyrimidine has not, so far, well defined. The existence of a presynaptic purinergic modulation of trasmitter release in the central nervous system (1) emphasize a possibly important role ...
P. Cardelli Cangiano   +4 more
openaire   +4 more sources

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