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:3.5.1.5 (urease)
7,257 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Helicobacter pylori produces a 550 kDa, multimeric, nickel-containing urease that catalyses the hydrolysis of urea to yield ammonia and carbonic acid. The ure gene cluster, comprised of seven genes, encodes the two structural subunits UreA (26.5 kDa) and UreB (60.3 kDa), and five accessory proteins: UreI, UreE, UreF, UreG and UreH. Accessory proteins are required for nickel ion insertion into the apoenzyme. The native protein consists of six copies each of UreA and UreB; two nickel ions are coordinated into each UreB active site. Urease is found in the cytosol, but may also localize on the surface (although this may be an artefact) and elicits a strong serum immunoglobulin response. Urease aids in colonization of the host by neutralizing gastric acid and providing ammonia for bacterial protein synthesis. Host defences are avoided by urease by continuing to neutralize acid locally and by shedding urease, which may be bound by immunoglobulin, from the surface of the bacterium. Host tissues can be damaged directly by the urease-mediated generation of ammonia and indirectly by urease-induced stimulation of the inflammatory response, including recruitment of leukocytes and triggering of the oxidative burst in neutrophils.
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PMID:The role of Helicobacter pylori urease in the pathogenesis of gastritis and peptic ulceration. 873 Feb 60

The gravity-sensing organ of Aplysia californica consists of bilaterally paired statocysts containing statoconia, which are granules composed of calcium carbonate crystals in an organic matrix. In early embryonic development, Aplysia contain a single granule called a statolith, and as the animal matures, statoconia production takes place. The objective of this study was to determine the effect of hypergravity on statoconia production and homeostasis and explore a possible physiologic mechanism for regulating this process. Embryonic Aplysia were exposed to normogravity or 3 x g or 5.7 x g and each day samples were analyzed for changes in statocyst, statolith, and body dimensions until they hatched. In addition, early metamorphosed Aplysia (developmental stages 7-10) were exposed to hypergravity (2 x g) for 3 weeks, and statoconia number and statocyst and statoconia volumes were determined. We also determined the effects of hypergravity on statoconia production and homeostasis in statocysts isolated from developmental stage 10 Aplysia. Since prior studies demonstrated that urease was important in the regulation of statocyst pH and statoconia formation, we also evaluated the effect of hypergravity on urease activity. The results show that hypergravity decreased statolith and body diameter in embryonic Aplysia in a magnitude-dependent fashion. In early metamorphosed Aplysia, hypergravity decreased statoconia number and volume. Similarly, there was an inhibition of statoconia production and a decrease in statoconia volume in isolated statocysts exposed to hypergravity in culture. Urease activity in statocysts decreased after exposure to hypergravity and was correlated with the decrease in statoconia production observed. In short, there was a decrease in statoconia production with exposure to hypergravity both in vivo and in vitro and a decrease in urease activity. It is concluded that exposure to hypergravity downregulates urease activity, resulting in a significant decrease in the formation of statoconia.
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PMID:A mechanism of adaptation to hypergravity in the statocyst of Aplysia californica. 895 50

Statoconia are calcium carbonate inclusions in the lumen of the gravity-sensing organ, the statocyst, of Aplysia californica. The aim of the present study was to examine the role of carbonic anhydrase and urease in statoconia mineralization in vitro. The experiments were performed using a previously described culture system (Pedrozo et al., J. Comp. Physiol. (A) 177:415-425). Inhibition of carbonic anhydrase by acetazolamide decreased statoconia production and volume, while inhibition of urease by acetohydroxamic acid reduced total statoconia number, but had no affect on statoconia volume. Inhibition of carbonic anhydrase initially increased and then decreased the statocyst pH, whereas inhibition of urease decreased statocyst pH at all times examined; simultaneous addition of both inhibitors also decreased pH. These effects were dose and time dependent. The results show that carbonic anhydrase and urease are required for statoconia formation and homeostasis, and for regulation of statocyst pH. This suggests that these two enzymes regulate mineralization at least partially through regulation of statocyst pH.
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PMID:Regulation of statoconia mineralization in Aplysia californica in vitro. 908 70

Yersinia enterocolitica produces the enzyme urease which hydrolyses urea, resulting in the production of carbonic acid and ammonia and a net increase in pH. In the presence of urea, urease enhances survival of Y. enterocolitica in the stomach and presumably in other acidic environments the bacteria encounter during the course of infection. In this study we show that Y. enterocolitica urease is a cytosolic enzyme which has a low Km value (0.15 +/- 0.01 mM urea), suggesting that it functions at close to maximum velocity even at the low concentrations of urea available to Y. enterocolitica in gastric fluid and other tissues. Y. enterocolitica urease was active over a wide pH range, but unlike most other bacterial ureases, displayed an optimal activity at pH 3.5-4.5, suggesting a physiological role in protecting the bacteria from acid. Higher levels of urease activity were attained at 28 degrees C than at 37 degrees C, and investigation of the regulation of urease production revealed that the enzyme was not induced by urea, or by nitrogen limitation. Instead maximal activity was attained during the stationary phase of growth which coincides with the period of maximum acid tolerance of the bacteria. This type of regulation has not been described for any other ureolytic bacteria and seems to be unique to Y. enterocolitica.
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PMID:A novel mechanism of urease regulation in Yersinia enterocolitica. 911 97

To better understand the mechanisms that could modulate the formation of otoconia, calcium carbonate granules in the inner ear of vertebrate species, we examined statoconia formation in the gravity-sensing organ, the statocyst, of the gastropod mollusk Aplysia californica using an in vitro organ culture model. We determined the type of calcium carbonate present in the statoconia and investigated the role of carbonic anhydrase (CA) and urease in regulating statocyst pH as well as the role of protein synthesis and urease in statoconia production and homeostasis in vitro. The type of mineral present in statoconia was found to be aragonitic calcium carbonate. When the CA inhibitor, acetazolamide (AZ), was added to cultures of statocysts, the pH initially (30 min) increased and then decreased. The urease inhibitor, acetohydroxamic acid (AHA), decreased statocyst pH. Simultaneous addition of AZ and AHA caused a decrease in pH. Inhibition of urease activity also reduced total statoconia number, but had no effect on statoconia volume. Inhibition of protein synthesis reduced statoconia production and increased statoconia volume. In a previous study, inhibition of CA was shown to decrease statoconia production. Taken together, these data show that urease and CA play a role in regulating statocyst pH and the formation and maintenance of statoconia. CA produces carbonate ion for calcium carbonate formation and urease neutralizes the acid formed due to CA action, by production of ammonia.
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PMID:Evidence for the involvement of carbonic anhydrase and urease in calcium carbonate formation in the gravity-sensing organ of Aplysia californica. 926 17

Urea diffusing from saliva into dental plaque is converted to ammonia and carbon dioxide by bacterial ureases. The influence of normal salivary urea levels on the pH of fasted plaque and on the depth and duration of a Stephan curve is uncertain. A numerical model which simulates a cariogenic challenge (a 10% sucrose rinse alone or one followed by use of chewing-gum with or without sugar) was modified to include salivary urea levels from 0 to 30 mmol/l. It incorporated: site-dependent exchange between bulk saliva and plaque surfaces via a salivary film; sugar and urea diffusion into plaque; pH-dependent rates of acid formation and urea breakdown; diffusion and dissociation of end-products and other buffers (acetate, lactate, phosphate, ammonia and carbonate); diffusion of protons and other ions; equilibration with fixed and mobile buffers; and charge-coupling between ionic flows. The Km (2.12 mmol/l) and Vmax (0.11 micromol urea/min/mg dry weight) values for urease activity and the pH dependence of Vmax were taken from the literature. From the results, it is predicted that urea concentrations normally present in saliva (3-5 mmol/l) will increase the pH at the base of a 0.5-mm-thick fasted plaque by up to 1 pH unit, and raise the pH minimum after a sucrose rinse or sugar-containing chewing-gum by at least half a pH unit. The results suggest that plaque cariogenicity may be inversely related to salivary urea concentrations, not only when the latter are elevated because of disease, but even when they are in the normal range.
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PMID:A mathematical model of the influence of salivary urea on the pH of fasted dental plaque and on the changes occurring during a cariogenic challenge. 943 74

Calcium phosphate is deposited in many diseases, but formation mechanisms remain speculative. Nanobacteria are the smallest cell-walled bacteria, only recently discovered in human and cow blood and commercial cell culture serum. In this study, we identified with energy-dispersive x-ray microanalysis and chemical analysis that all growth phases of nanobacteria produce biogenic apatite on their cell envelope. Fourier transform IR spectroscopy revealed the mineral as carbonate apatite. The biomineralization in cell culture media resulted in biofilms and mineral aggregates closely resembling those found in tissue calcification and kidney stones. In nanobacteria-infected fibroblasts, electron microscopy revealed intra- and extracellular acicular crystal deposits, stainable with von Kossa staining and resembling calcospherules found in pathological calcification. Previous models for stone formation have led to an hypothesis that elevated pH due to urease and/or alkaline phosphatase activity is a lithogenic factor. Our results indicate that carbonate apatite can be formed without these factors at pH 7.4, at physiological phosphate and calcium concentrations. Nanobacteria can produce apatite in media mimicking tissue fluids and glomerular filtrate and provide a unique model for in vitro studies on calcification.
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PMID:Nanobacteria: an alternative mechanism for pathogenic intra- and extracellular calcification and stone formation. 965 77

The most important phosphates involved in urinary stone disease are carbonate apatite, brushite, and struvite. Overall, phosphate stones account for 12-20% of all stones, with a downward trend for struvite and an increase in carbonate apatite being observed in the last decade. The physicochemical basis for the formation of phosphate calculi is supersaturation. Once the solubility product has been exceeded, a metastable process of supersaturation begins, with slow crystalline growth. If a critical limit of supersaturation is exceeded, large-scale spontaneous precipitation of crystals occurs in a second stage. No urinary tract infection is involved in brushite stone formation. Although infection is not a prerequisite for the formation of carbonate apatite stones, infective conditions favor carbonate apatite formation. Struvite is the characteristic infection calculus, formed as a result of urinary tract infection with urease-producing bacteria. During the first episode of urinary stone disease a definitive diagnosis of the type of stone involved is very difficult without analysis of the latter by infrared spectroscopy or X-ray diffraction. In recurrent disease, appropriate treatment can be initiated on the basis of the previous stone analysis in the majority of cases. The best means of preventing recurrent disease involving any type of phosphate stone is definitive calculus removal by shock-wave lithotripsy, percutaneous stone removal, or open surgery (especially in children). Chemolysis via acidification of the urine with Suby G solution or hemicidrin supported by oral acidification, achieved by the metabolism of L-methionine, and antibiotic therapy (especially for infectious stones) are important adjuvant modalities of therapy. After therapy of phosphate stones, metaphylaxis involving controlled urinary acidification with L-methionine supports the treatment of infection and, at a pH value of less than 6.2 and urine dilution to 2.5 l/24 h, prevents the crystallization of struvite, brushite, and carbonate apatite.
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PMID:Causes of phosphate stone formation and the importance of metaphylaxis by urinary acidification: a review. 1055 50

Catalytic decomposition of urea by urease in aqueous calcium chloride solutions was used to rapidly prepare calcium carbonate polymorphs at room temperature. The nature of the resulting particles depended on the concentration of the enzyme and, in a strong manner, on the agitation of the reacting solutions. In an undisturbed system an amorphous precipitate is formed first, which readily crystallized to vaterite and upon aging changed to calcite. Under the influence of magnetic stirring, the amorphous phase could be not observed; instead smaller particles were initially obtained, which aggregated to vaterite and calcite. Similarly, the application of ultrasonic energy produced small vaterite particles at the early stages. It is apparent that enzyme macromolecules are important in the development of calcite faces and, as such, they exert significant influence on calcite morphology, without being present in detectable amounts in the resulting solids. Copyright 2001 Academic Press.
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PMID:Homogeneous Precipitation of Calcium Carbonates by Enzyme Catalyzed Reaction. 1135 Jan 56

No intravenously injectable enzyme preparate containing urease as an alternetive to hemodialysis, hemoperfusion and CAPD systems in patients having chronic renal failure has been encountered in literature. In this study, it has been aimed to convert blood urea to alanine by using PEG-urease/PEG-AlaDH enzyme pair encapsulated within living erythrocyte. In this system, urea is decomposed into NH3 and HCO3- and the ammonia released is converted into alanine by reacting pyruvate under the catalytic action of alaninedehydrogenase. The production of pyruvate and NADH by erythrocyte required in the second stage of the reaction will make the process a feasible and ceaseless one. The success of the system will enable the renal patients with diabetes mellitus. Urease and AlaDH were covalently immobilized on activated PEG. PEG-urease/PEG-AlaDH were encapsulated in erythrocyte (1/1)(v/v) by using slow dialysis methods. The activity of enzyme system, encapsulation yield and hemogram analysis were determined for each sample.
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PMID:Encapsulation of PEG-urease/PEG-AlaDH enzyme system in erythrocyte. 1170 64


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