Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:6.3.4.6 (urease)
7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The final products of the arginine catabolism that can be utilized as a nitrogen source in Neurospora crassa are ammonium, glutamic acid, and glutamine. The effect of these compounds on arginase induction by arginine was studied. In wild-type strain 74-A, induction by arginine was almost completely repressed by glutamic acid plus ammonium, whereas ammonium or glutamic acid alone had only moderate effects. Arginine products of catabolism also repressed arginase induction. A mutant, ure-1, which lacks urease activity, hyperinduced its arginase with arginine as a nitrogen source. The addition of either ammonium or glutamine produced effects similar to those in the wild-type strain. The effect of ammonium on arginase induction is mediated through its conversion into glutamine. This was demonstrated in mutant am-1, which lacks L-glutamate dehydrogenase activity. In this mutant, the effect of glutamic acid was reduced, and, with ammonium, it was completely lost. The addition of glutamine or glutamic acid plus ammonium to this strain decreased by threefold the induction of arginase by arginine. Proline, a final product of arginine catabolism, competitively inhibited arginase activity. This effect and the repression of arginase by glutamine are examples of negative modulation of the first enzyme in a catabolic pathway by its final products.
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PMID:Nitrogen regulation of arginase in Neurospora crassa. 14 62

Constitutivity for the synthesis of the urea amidolyase bienzymatic complex is obtained by durOh mutations located in the regulatory genetic region adjacent to the dur1, dur2 gene cluster. The durOh mutations act only in cis and are a new case of cis effect strongly cancelled in alpha/a diploid, similar to cargA+Oh mutation shown previously to lead to arginase constitutivity. Illegitimate diploids do not show such a cancellation of constitutivity. The constitutivity produced by durOh mutation comprises the process of induction and the release of the glutamine effect. It does not impair the NH+4 effect.
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PMID:The regulation of urea amidolyase of Saccharomyces cerevisiae: mating type influence on a constitutivity mutation acting in cis. 36 77

Twenty amino acids were examined for their effects on urinary orotic acid excretion. Except for arginine and ornithine, all of the remaining amino acids tested induced a mild orotic aciduria in rats 2 hours post feeding. Two ammonium salts, and urease also acted, as inducers of orotic aciduria. The ammoneogenic properties of the amino acids tested could not solely explain the induced excretion of orotic acid. Only serine, glutamine, NH4Cl, (NH4)2CO3, and urease increased orotic acid excretion in the 24 hour fasted rat. Administration of 0.5 mmoles of arginine or ornithine ameliorated the mild orotic aciduria induced by either glycine or lysine. Arginine was shown to be more efficacious in preventing glycine induced orotic aciduria than was ornithine. Amino acid induced orotic aciduria is dependent upon the physiological state of the animal, varying with the state of digestion and the supply of arginine.
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PMID:Amino acid induced orotic aciduria. 63 45

In an attempt to understand the role of nickel in jack bean urease (1), we turned to a variety of other enzymes important in the utilization, production, or transfer of ammonia. We found several, including the L-histidine and L-phenylalanine ammonialyases and some enzymes that utilize glutamine or ammonia in amidotransferase reactions, all of which show evidence for the involvement of as yet unreported transition metal ions in their mechanism of action. We support the view that catalysis by metalloenzymes may be a reflection of the chemistry of the metal ion itself as a Lewis acid, and that perhaps too much emphasis has been placed on supposed special characteristics (such as strains, "entasis") of the enzyme-metal ion association. In this context, we have discussed the mechanism of catalysis of hydrolysis of specific substrates by carboxypeptidase A, and have returned to urease to examine the role of nickel in its mechanism of action.
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PMID:Metal ions in enzymes using ammonia or amides. 76 57

Nitrogen-free analogues of essential amino acids, when administered with those essential amino acids for which analogues are ineffective or unavailable, exert three actions that may be beneficial in protein-deficient or protein-intolerant subjects. First, they bring about an increase in the concentrations of essential amino acids in the blood at the expense of the concentrations of certain non-essential amino acids, notably alanine and glutamine. This effect is most readily demonstrated in children with congenital defects of the urea cycle enzymes, but can also be seen during daily therapy of adults with portal-systemic encephalopathy. Second, these compounds promote nitrogen balance through their suppressive effect on urea synthesis (an effect not attributable to re-utilization of ammonia derived from urease action in the gut). This action is demonstrable in obese subjects who are already conserving nitrogen maximally at the end of a prolonged fast and can also be shown in the first week of fasting when the branched-chain keto acids alone are administered. In both situations, improved nitrogen conservation persists long after the analogues are metabolized, suggesting enzyme adaptations. In chronic uremics, nitrogen balance can be maintained in some (but not all) patients on very low nitrogen intakes. Third, these mixtures may delay or reverse the progressive decline in glomerular filtration rate characteristic of chronic renal failure in some cases: thus, for example, 5 of 6 patients taken off chronic dialysis have maintained lower serum urea concentrations without evidence of protein malnutrition for periods of 2-24 months.
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PMID:Evidence for an anabolic action of essential amino acid analogues in uremia and starvation. 107 39

The energy-dependent urea permease was studied in two strains of Pseudomonas aeruginosa, measuring the uptake (transport and metabolism) of 14C-urea. In both strains urea uptake in vivo and urease activity in vitro differed significantly with respect to kinetic parameters, temperature and pH dependence and response to metabolic inhibitors. Ammonium strongly interfered both with the expression of the urea uptake system and its activity. The inhibition of the uptake activity by ammonium was partially relieved by hydraziniumsulfate, which prevented the translocation of ammonium into the cell, and in a methylammonium/ammonium transport-defective mutant of strain DSM 50071. Furthermore, methionine-sulfoximine, which prevented the intracellular glutamine formation from ammonium via inhibition of glutamine synthetase, relieved the inhibition of urea uptake by ammonium. These findings suggested that urea uptake activity in P. aeruginosa is regulated by intracellular glutamine.
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PMID:Regulation of urea uptake in Pseudomonas aeruginosa. 135 27

The middle base (U35) of the anticodon of tRNA(Gln) is a major element ensuring the accuracy of aminoacylation by Escherichia coli glutaminyl-tRNA synthetase (GlnRS). An opal suppressor of tRNA(Gln) (su+2UGA) containing C35 (anticodon UCA) was isolated by genetic selection and mutagenesis. Suppression of a UGA mutation in the E. coli fol gene followed by N-terminal sequence analysis of purified dihydrofolate reductase showed that this tRNA was an efficient suppressor that inserted predominantly tryptophan. Mutations of the 3-70 base pair (U70 and A3U70) were made. These mutants of su+2UGA are less efficient suppressors and inserted predominantly tryptophan in vivo; alanine insertion was not observed. Mutations of the discriminator nucleotide (A73, U73, C73) result in very weak opal suppressors. Aminoacylation in vitro by E. coli TrpRS of tRNA(Gln) transcripts mutated in the anticodon demonstrate that TrpRS recognizes all three nucleotides of the anticodon. The results show the interchangeability of the glutamine and tryptophan identities by base substitutions in their respective tRNAs. The amber suppressor (anticodon CUA) tRNA(Trp) was known previously to insert predominantly glutamine. We show that the opal suppressor (anticodon UCA) tRNA(Gln) inserts mainly tryptophan. Discrimination by these synthetases for tRNA includes position 35, with recognition of C35 by TrpRS and U35 by GlnRS. As the use of the UGA codon as tryptophan in mycoplasma and in yeast mitochondria is conserved, recognition of the UCA anticodon by TrpRS may also be maintained in evolution.
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PMID:Switching tRNA(Gln) identity from glutamine to tryptophan. 156 39

Using in vivo 1H NMR spectroscopy (1H MRS) and biochemical analysis, the effects of hyperammonemia on cerebral function were studied in three rat models: acute liver ischemia (LIS), administration of urease (UREASE) and administration of methionine sulfoximine (MSO). By means of localization in three dimensions signals were obtained exclusively from the cerebral cortex. Specially developed lineshape correction and fitting methods were used to quantitate the MRS signals. The following concentration changes were observed; a decrease in glutamate and (phospho)choline for all the models; an increase in glutamine in the LIS and UREASE model but a decrease in the MSO model; a marked increase in lactate in the LIS and UREASE group; a tendency to a decrease in N-acetylaspartate in all the models. These changes agree well with the changes in the post-mortem biochemically determined cerebral cortex glutamine and glutamate concentrations. Estimated absolute 1H MRS metabolite concentrations agree well with those obtained by other techniques; cerebral cortex glutamate, however, is underestimated by about 35% by NMR. The present data support the hypothesis that hyperammonemia is associated with a decreased availability of glutamate for neurotransmission.
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PMID:The use of in vivo proton NMR to study the effects of hyperammonemia in the rat cerebral cortex. 167 7

At present in vivo NMR spectroscopic studies of brain glutamate and glutamine concentrations relative to encephalopathy have mainly been performed in hepatic encephalopathy (HE). In vivo proton NMR studies were performed in rats with hyperammonemia and acute HE due to acute liver ischemia as well as in rats with hyperammonemia due to either repeated urease i.p. injection or i.p. administration of methionine sulfoximine, a well known inhibitor of glutamine synthetase. In man, in vivo proton NMR is described in patients with chronic liver disease: cirrhosis of different etiology and associated with different degrees of HE. In the experimental models proton NMR spectroscopy of the cerebral cortex revealed an increase in glutamine concentration, a decrease in glutamate concentration and a decrease in phosphocholine compounds. In humans no clear distinction between cerebral cortex glutamate and glutamine concentration could be made by in vivo 1H NMR spectroscopy. However, the combined glutamate/glutamine peak increased in a way compatible with an increased cerebral cortex glutamine concentration during chronic HE. In the cirrhotic patients too a decrease in cerebral cortex phosphocholine compounds was observed, the explanation of which is unclear. Both the experimental work and the clinical observations support the hypothesis that impairment of the glutamate/glutamine cycle between astrocytes and neurons plays a role in the pathogenesis of hepatic encephalopathy.
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PMID:What the clinician can learn from MR glutamine/glutamate assays. 167 85

1. Portacaval shunting in rats results in several metabolic alterations similar to those seen in patients with hepatic encephalopathy. The characteristic changes include: (a) diminution of cerebral function; (b) raised plasma ammonia and brain glutamine levels; (c) increased neutral amino acid transport across the blood-brain barrier; (d) altered brain and plasma amino acid levels; and (e) changes in brain neurotransmitter content. The aetiology of these abnormalities remains unknown. 2. To study the degree to which ammonia could be responsible, rats were made hyperammonaemic by administering 40 units of urease/kg body weight every 12 h and killing the rats 48 h after the first injection. 3. The changes observed in the urease-treated rats were: (a) whole-brain glucose use was significantly depressed, whereas the levels of high-energy phosphates remained unchanged; (b) the permeability of the blood-brain to barrier to two large neutral amino acids, tryptophan and leucine, was increased; (c) blood-brain barrier integrity was maintained, as indicated by the unchanged permeability-to-surface-area product for acetate; (d) plasma and brain amino acid concentrations were altered; and (e) dopamine, 5-hydroxytryptamine (serotonin) and noradrenaline levels in brain were unchanged, but 5-hydroxyindoleacetic acid (5-HIAA), a metabolite of 5-hydroxytryptamine, was elevated. 4. The depressed brain glucose use, increased tryptophan permeability-to-surface-area product, elevated brain tryptophan content and rise in the level of cerebral 5-HIAA were closely correlated with the observed rise in brain glutamine content. 5. These results suggest that many of the metabolic alterations seen in rats with portacaval shunts could be due to elevated ammonia levels. Furthermore, the synthesis or accumulation of glutamine may be closely linked to cerebral dysfunction in hyperammonaemia.
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PMID:Hyperammonaemia causes many of the changes found after portacaval shunting. 170 23


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