Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Monoamine oxidase activity in platelets prepared from the blood of patients with iron-deficiency anaemia was significantly lowered when compared with that in platelets from normal subjects. 2. The Km values of the platelet enzyme for the substrates dopamine, 5-hydroxytryptamine, phenylethylamine and kynuramine were similar for the platelet enzyme from iron-deficient and normal groups. 3. Heat-in-activation studies showed that the platelet monoamine oxidase from iron-deficient subjects was more labile to this treatment, when compared with the platelet enzyme from normal subjects. 4. The sensitivity of platelet monoamine oxidase to the inhibitors, clorgyline and deprenil, was increased in iron-deficiency anaemia. 5. Binding studies with the 14C-binding irreversible monoamine oxidase inhibitor, deprenil, showed that the amount of enzyme capable of binding this inhibitor was lowered by 48% in platelets from iron-deficient patients when compared with platelets from normal subjects. 6. The results show that there is a lowered amount of active enzyme in platelets from iron-deficient subjects. It is suggested that iron is necessary either for the synthesis of monoamine oxidase apoenzyme or is a cofactor for an enzyme which attaches flavin-adenine dinucleotide covalently to the monoamine oxidase apoenzyme.
Clin Sci Mol Med 1976 Jun
PMID:Some properties of human platelet monoamine oxidase in iron-deficiency anaemia. 0 85

1. Patients with sickle-cell anaemia were unable to increase free water reabsorption (TcH2O) in response to intravenous hypertonic sodium chloride solution. 2. Ethacrynic acid caused a brisk natriuresis in patients with sickle-cell anaemia but fractional sodium excretion was lower in these patients. 3. These findings could be explained by abnormal function of the loop of Henle.
Clin Sci Mol Med 1977 Dec
PMID:Excretion of salt and water by patients with sickle-cell anaemia: effect of a diuretic and solute diuresis. 58 37

1. Ventilation and cardiac frequency were measured during repeated treadmill exercise in three healthy subjects over 36 weeks, before, during and after iron-deficiency anaemia was produced and after iron treatment. The haemoglobin and 2,3-diphosphoglycerate concentrations and the oxygen-binding (P50) were measured. 2. There was an inverse relationship between the haemoglobin concentrations and the 2,3-diphosphoglycerate concentrations and the P50 values. 3. The mean cardiac frequencies during the fourth to tenth minutes of exercise showed a negative correlation with the haemoglobin concentrations in all three subjects, and the mean minute ventilations in two of them.
Clin Sci Mol Med 1977 Dec
PMID:Anaemia, iron deficiency and exercise: extended studies in human subjects. 58 38

1. Mice were infected with fertile bisexual Schistosoma mansoni and compared with similar animals infected with unisexual worms or sterile bisexual worms. 2. A significant increase in splenic weight occurred in all infected animals. 3. Administration of well-tolerated doses of 6-mercaptopurine abolished the increase in relative splenic weight in animals infected with ordinary S. mansoni. 4. In splenectomized uninfected mice leucocytosis but no other haematological changes developed. 5. In splenectomized mice lower values for packed cell volume were observed 8 weeks after, but not 12 weeks after, infection with S. mansoni. 6. Slight prolongation of the life-span of erythrocytes occurred in splenectomized infected mice. 7. It is concluded that anaemia in schistosomiasis depends to a significant extent on immunity developed to adult schistosomal worms and can develop in the absense of schistosomal ova. 8. The anaemia resulting from such an immune response may be suppressed by administration of 6-mercaptopurine. 9. Such anaemia occurs even in splenectomized mice; thus hypersplenism is not necessary for its development although splenectomy slightly prolongs the erythrocyte life-span.
Clin Sci Mol Med 1978 Apr
PMID:The causation of splenomegaly in schistosomiasis in mice. 63 70

1. In a series of patients with sickle-cell anaemia, serum phosphate and magnesium concentrations were elevated. Serum calcium concentrations were normal. Urinary excretion of calcium was decreased. 2. The maximum tubular reabsorption of phosphate per litre of glomerular filtrate (TmP/GFR) was significantly increased in these patients. 3. The increase in phosphate reabsorption explains the elevated serum phosphate observed in these patients.
Clin Sci Mol Med 1978 Nov
PMID:The tubular reabsorption of phosphate in sickle-cell nephropathy. 71 96

1. The activity of monoamine oxidase, when assayed with four substrates, was significantly lowered in platelets prepared from the blood of patients with iron-deficiency anaemia. 2. Treatment with oral iron preparations restored platelet monoamine oxidase activity to normal in those patients whose serum iron concentrations also returned to normal. 3. Platelet monoamine oxidase activity remained low if treatment failed to restore serum iron concentration to within normal limits.
Clin Sci Mol Med 1975 Apr
PMID:Human platelet monoamine oxidase activity in iron-deficiency anaemia. 112 21

1. Six unanaesthetized goats were used to evaluate the effect of liver failure on the hypoxic responsiveness of cerebral blood flow. The animals breathed air and several different hypoxic gas mixtures enriched with sufficient CO2 to maintain an isocapnic state. The cerebral metabolic rate for O2 (CMRo2) was also measured in four of these goats. 2. In baseline studies there was a linear relationship between cerebral blood flow and arterial O2 saturation (Sa,o2) measured at different levels of isocapnic hypoxia. The slopes of the cerebral blood flow/Sa,o2 response lines were used to quantify the response of cerebral blood flow to hypoxia. In the healthy goat, CMRo2 was not depressed by hypoxia until the O2 tension (Po2) in arterial and cerebral venous blood had fallen below critical threshold values of approximately 3-2 and 2-2 kPa (24 and 16 mmHg) respectively. 3. Liver failure was accompanied by a fall in cerebral blood flow and CMRo2. There was also a depression in the response of cerebral blood flow to hypoxia and a disproportionate reduction of cerebral O2 delivery in hypoxia. CMRo2 was further reduced at arterial and cerebral venous Po2 values, which were much higher than the critical threshold values for producing hypoxic CMRo2 depression in health. 4. It is concluded that the brain becomes more vulnerable to the adverse effects of hypoxia during liver failure. This may be of practical importance in the management of patients with arterial hypoxaemia or other complications (e.g. anaemia or shock), which may reduce cerebral oxygen delivery.
Clin Sci Mol Med 1976 Jan
PMID:Effect of liver failure on the cerebral circulatory and metabolic responses to hypoxia in the goat. 124

Recent linkage studies located genes responsible for the low voltage EEG, benign neonatal convulsions and for the Fanconi anaemia to the vicinity of the VNTR marker CMM6 (D20S19). Physical mapping experiments using pulsefield electrophoresis in the distal part of chromosome 20q were chosen as a first step towards cloning of these genes. The observed pattern of shared fragments lead to the locus order 'tel-IP20K09-RMR6-CMM6-MS214-cen', which differs from previously reported genetic linkage maps. The physical intervals between these probes are markedly shorter compared with the genetic distances. Clusters of rare cutter sites around CMM6 point to at least four closely related CpG islands.
Hum Mol Genet 1992 Aug
PMID:D20S19, linked to low voltage EEG, benign neonatal convulsions, and Fanconi anaemia, maps to a region of enhanced recombination and is localized between CpG islands. 130 9

The detection of the single base pair mutations at codon 6 of the beta-globin gene is important for the prenatal diagnosis of sickle-cell anaemia and SC disease. A novel procedure has been designed to create a restriction site at both the beta A and beta C alleles to facilitate the discrimination of haemoglobins A, S and C. The general principle of this procedure is to enzymatically amplify genomic DNA using a modified primer containing an altered 3'-terminal nucleotide to create these restriction sites. After this modified primer has been efficiently incorporated into amplified DNA, the PCR products are digested with the restriction enzymes Ava I and Sty I. Ava I recognizes a site in amplified DNA containing a beta A allele, and Sty I recognizes a site in DNA containing a beta C allele. Since the beta A and beta C alleles can be distinguished directly by the presence of a restriction site, the beta S allele can be identified indirectly. All three beta-globin alleles are easily distinguished by size and pattern of electrophoresed fragments on agarose gels. This procedure is specific and sensitive, thus permitting rapid, economical diagnosis of sickle-cell anaemia and SC disease.
Mol Cell Probes 1992 Aug
PMID:Prenatal diagnosis by enzymatic amplification and restriction endonuclease digestion for detection of haemoglobins A, S and C. 132 16

We previously demonstrated that 3'-azido-3'-deoxythymidine (AZT) inhibits hemoglobin (Hb) synthesis and globin gene transcription in butyric acid-induced K-562 leukemia cells, suggesting that these effects may play a role in the AZT-induced anemia observed in patients [Mol. Pharmacol. 38:797-804 (1990)]. The recent discovery by our group of a novel metabolite of AZT. 3'-amino-3'-deoxythymidine (AMT), which exhibits a high degree of toxicity toward human hemopoietic cells [Mol. Pharmacol. 39:258-266 (1991); Antimicrob. Agents Chemother. 35:801-807 (1991)], has led us to explore potential effects of this AZT metabolite on Hb production, globin mRNA expression, and heme synthesis in butyric acid-induced K-562 human erythroleukemia cells. AMT inhibited Hb synthesis by approximately 21%, as measured by benzidine staining, at concentrations as low as 25 microM, with slightly increased inhibition at higher AMT concentrations. The inhibition of Hb production by AMT was substantially lower, compared with that of AZT. AMT inhibited globin mRNA steady state levels in a dose-dependent manner to a similar extent as did the parent drug, with approximately 50% inhibition by each compound at a concentration of 100 microM. Nuclear run-on transcription assays demonstrated that inhibition by AMT of globin mRNA synthesis was associated with a decreased rate of globin-specific gene transcription. Globin mRNA stability was not affected by either 100 microM AZT or AMT, as measured after blockage of transcription with actinomycin D. To gain insight into potential mechanism(s) responsible for the different quantitative effects of AZT and AMT on Hb synthesis, the effect of each compound on induction of heme synthesis in K-562 cells was determined. Although heme induction was not affected by AMT, a significant inhibition approximating 20% was observed in the presence of 100 microM AZT. In addition, AZT down-regulated mRNA steady state levels under conditions where heme synthesis was inhibited by succinylacetone. These data suggest that inhibition by AZT of globin gene expression is a direct effect and is not secondary to inhibition of heme synthesis. This study emphasizes the role of AMT in the pharmacodynamic properties of AZT, in relation to its toxicity, and suggest that both AMT and AZT may be involved in the inhibition of erythroid differentiation observed in vivo, through changes in gene expression.
Mol Pharmacol 1992 Feb
PMID:Comparative effects of 3'-azido-3'-deoxythymidine and its metabolite 3'-amino-3'-deoxythymidine on hemoglobin synthesis in K-562 human leukemia cells. 153 5


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