Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the search for gastric ATPases that might be related to the mechanism of HCl secretion, an interesting and rather unique K+-stimulated ATPase has been discovered. This enzyme is isolated from oxyntic cells and has been associated with the apical plasma membrane and/or tubulovesicular system. Membrane vesicles containing the K+-stimulated ATPase transport H+ into the vesicular lumen under the appropriate conditions of ATP, Mg2+, and KCl. This process can be measured by pH electrode, binding of certain metachromatic dyes to "energized" sites, or accumulation ratios of substances with appropriate pK values. Vesicular interior can be acidified to pH 3.5 or below. At the present time, it is difficult to distinguish between an electrogenic H+ pump and an electroneutral H+/K+ exchange mechanism. A hypothetical scheme for the gastric H+ secretory mechanism is proposed which fits much of the data from studies on the K+-ATPase, vesicular transport, and intact gastric mucosa.
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PMID:Gastric adenosine triphosphatases: a review of their possible role in HCl secretion. 2 Mar 86

The Na-K-ATPase-activity of the isolated, cell-free perfused rat kidney was investigated. Na-load and perfusion rate could be varied independently. The ATPase-assay was carried out on plasmamembranes (700-1200 g fraction) isolated and purified after 60 min perfusion. Both the specific Na-K-ATPase-activity and the fractional Na-reabsorption showed an indirect correlation with the Na-load as well as with the perfusion rate. The Na-K-ATPase-activity of plasmamembranes obtained from the isolated kidney at physiological Na-load fits well to control values prepared from unperfused control kidneys. The present data are in accord with the results of earlier micropuncture experiments, where acute saline loading diminished the rate of Na-absorption.
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PMID:Acute changes of the Na-K-ATPase-activity in plasmamembranes of the isolated, cell-free perfused rat kidney. 12 58

The total Mg2+-ATPase and Na+, K+-ATPase activity was studied in the fractions of "400 g X for 20 min" and "900 g X for 30 min" conditionally called the fraction of the external cellular membranes and total fraction of mitochondria. The subcellular fractions were isolated from great hemispheres and stem part of the rat brain. The brain of control animals and those during a severe spasmodic attact induced by the oxygen action at a pressure of 6 ati was studied. The total ATPase activity is established to be practically the same in the studied brain areas and unchanged with hyperoxia. Hyperoxia accompanying by convulsions results in an increase in the activity of Mg2+-ATPase and in a decrease in that of Na+, K+-ATPase both in the cerebral cortex and the stem part. The authors suppose that the decrease in the enzyme activity may occur due to an inhibitory effect on it of the lipids reoxidation products formed in the brain with hyperoxia.
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PMID:[ATPase activity of subcellular rat brain fractions following hyperoxia]. 13 79

Actin-like (A-L) fraction from normal E. coli was compared with the protein from a potassium-transport mutant strain, and the cell-swelling reaction of both strains was studied. Findings were: (a) The membrane fraction of the mutant by SDS electrophoresis is deficient in the A-L fragment relative to normal whereas the soluble supernatant contains an excess. (b) Important catalytic differences exist between the A-L fractions of the two strains. The parent strain accumulates potassium in low K+ and the A-L fraction polymerizes in low K+. But the A-L fraction from the mutant fails to polymerize in low K media in the K+ concentration region where the mutant fails at K+ uptake. (c) The parent cell swells during low K+ uptake whereas the mutant does not. It is constructed from this that the differences in the characterization of A-L fraction relative to normal are related to the loss of cell-swelling in the mutant and hence to the loss in alkali cation selectivity. Thus two physical mechanisms, one macroscopic and dependent on the Gregor relation for swelling equilibria in ion exchange resins, and one more microscopic based on the dielectric dependence of the coulomb force between ion pairs, could underly regulation of ion selectivity by cell swelling. A similar proposal is made for the regulation of electron transport and oxidative phosphorylation in mitochondria. These findings and interpretations justify a new hypothesis to the effect that cell hydration is regulated by contractile proteins. The hypothesis fits together important observations hitherto unexplained, to wit: (1) The "missing link" as to the role of intermediate metabolism in biological ion exchange. (2) The swelling of bacterial protoplasts and its relation to (Mg2 + Ca2+)ATPase activity. (3) The swelling-contraction cycles of mitochondria and their role in electron transport. (4) The role of ATPase's in transport. (5) The significance of actomyosin fibers in nerve endings. (6) The significance of altered actomyosin structures in the cancerous cell.
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PMID:Biological ion exchanger resins. X. The cytotonus hypothesis: biological contractility and the total regulation of cellular physiology through quantitative control of cell water. 13 62

Serial estimation of muscle and serum adenosine triphosphatase (ATPase) activity was performed in 16 healthy control patients and 32 cases with tetanus. There was no significant difference due to age and sex in muscle and serum ATPase activity between the normal and tetanus cases. Tetanus patients showed a marked increase in muscle and serum ATPase activity as compared to normal. The ATPase activity increased with the severity of convulsion and disease. There was increased mortality in tetanus patients having higher values of muscle and serum ATPase.
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PMID:Muscle and serum adenosine triphosphatase in patients suffering from tetanus. 15

The controlling effect of ATP, K+ and Na+ on the rate of (Na+ + K+)-ATPase inactivation by 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole (NBD-C1) is used for the mathematical modelling of the interaction of the effectors with the enzyme under equilibrium conditions. 1. Of a series of conceivable interaction models, designed without conceptual restrictions to describe the effector control of inactivation kinetics, only one fits the experimental data described in a preceding paper. 2. The model is characterized by the coexistence of two binding sites for ATP and the coexistence of two separate binding sites for K+ and Na+ on the enzyme-ATP complex. On the basis of this model, the effector parameters fitting the experimental data most closely are estimated by means of nonlinear least-squares fits. 3. The apparent dissociation constants for ATP fo the enzyme-ATP complex or of the enzyme-(ATP)2 complex are computed to lie near 0.0024 mM and 0.34 mM, respectively, irrespective of whether K+ and Na+ were absent or K+ and K+ plus Na+, respectively, were present in the experiments. 4. The origin of the high and the low affinity site for binding of ATP to the (Na+ + K+)-ATPase molecule is traced back to the coexistence of two catalytic centres which, although primarily equivalent as to the reactivity of their thiol groups with NBD-C1, are induced into anticooperative communication by ATP binding and thus show an induced geometric asymmetry. 5. On the basis of the interaction model outlined under item 2 the apparent dissociation constant for K+ or Na+ in the (K+ + Na+)-liganded enzyme-ATP complex are computed to be 1.7 mM and 3.5 mM, respectively. 6. The conclusions concerning the coexistence of two primarily equivalent but anticooperatively interacting catalytic centres and the coexistence of two separate ionophoric centres for Na+ and K+ correspond to the appropriate basic postulates of the flip-flop concept of (Na+ + K+)-ATPase mechanism.
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PMID:Mathematical modelling of ATP, K+ and Na+ interactions with (Na+ + K+)-ATPase occurring under equilibrium conditions. 21 31

It was shown that the phenomenon of inactivation of Na, K-ATPase of the non-purified fraction of the rat cortical synaptosomes under electroshock may be related to "modification" of the potassium active center of the enzyme. The anticonvulsant diazepam injected intramuscularly also inhibits Na, K-ATPase of the cerebral membranes. However, in subsequent electrical stimulation of the brain the drug activates Na, K-ATPase as compared to controls. Diazepam also abolishes clonic convulsions induced by electrical stimulation of the brain. At the same time it does not eliminate compensatory shifts in the activity of acetyl-cholinesterase of the rat cerebral and spinal synaptosomes, characteristic of electroshock. The results are discussed from the standpoint that inhibition of the activity of Na, K-ATPase of the nerve endings membranes may underlie the pathogenetic mechanism of the convulsive activity.
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PMID:[Na, K-ATPase activity of the meninges in electroshock and the action of the anticonvulsant agent, diazepam]. 21 51

1. The fluxes of Na were measured on isolated coprodeal mucosa at 1--220 mM-Na from hens on low (L) and high (H) Na diets with the purpose of finding the location and characteristics of Na sites activated in the cellular pathway by L. 2. The influx across the brush border, JNamc, and the transmural fluxes, JNasm and JNams, were determined. Effects on these fluxes of ouabain, 10(-3) M in the serosal solution, and amiloride, 10(-4) M in the mucosal solution, were studied for both dietary states. 3. JNamc was 5--22 (L) and 0--0.8 (H) muequiv/cm2.hr at 130 mM-Na corrected for the paracellular flux of Na. The JNamc (H) is tenfold smaller than found by Choshniak, Munck & Skadhauge (1977). This discrepancy is at present inexplicable. Amiloride completely inhibited JNamc (L). Preincubation in 0 or 130 mM-Na had no effect on JNamc. Ouabain reduced JNamc (L) by only about 37% after preincubation at 130 mM-Na. The Kt of JNamc was 5.1 (L) and 50.6 (H) mM-Na. 4. JNasm was 50 (H) and 61 (L) n-equiv/cm2.hr at 6.5 mM-Na. Ouabain increased JNasm by 360% in the low Na state. The increased JNasm was inhibited 74--100% by amiloride. This is interpreted as a ouabain induced Na-Na exchange at the basolateral Na-K-ATPase and an almost complete block of JNacm by amiloride. A similar exchange of Na at the basolateral membrane in the high-Na state was revealed by 'opening' the brush border for Na with monensin added to the mucosal solution. Amiloride in itself prevented a 50% recirculation of Na via the paracellular route and back across the cells in the low Na state. 5. JNams was 5.6 (L) muequiv/cm2.hr and 187 (L) microA/cm2 at 6.5 mM-Na. Amiloride reduced these values to 0.4 muequiv/cm2.hr and 5.8 microA/cm2. On addition of amiloride the transmural resistance in (L) coprodea at 130 mM-Na increased from 140 to 190 and it remained unchanged at 260 omega cm2 in (H) coprodea. The resistance of (L) birds, 163, was not affected by ouabain, 166 (L) omega cm2. 6. 20:1 NaCl dilution potentials at the mucosal side of 17--18 mV (L) and nearly zero (H) had half-times around 1 sec. Amiloride eliminated completely these diffusion potentials. The short half-time indicates a location in the brush border of sodium specific sites induced by the low-Na diet. This conclusion is oppsite to that described by Choshniak et al. (1977). 7. Ion selectivity, voltage--current and conductance--concentration relations in the presence of amiloride indicated a weakly cation selective and highly hydrated pathway, which was also thick and with neutral sites. This fits a paracellular route with the limiting barrier for ions at the tight junction.
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PMID:Sodium transport in the hen lower intestine. induction of sodium sites in the brush border by a low sodium diet. 46 29

Hereditary spongiform dystrophy in young children is characterised by macrocephaly with spasticity, convulsions and ultimately a decerebrate state and diffuse electroencephalographic changes. Histological examination of the brain remains essential for its diagnosis. A review of the ultrastructural studies reported by various authors complements the findings obtained by conventional histology. We have thus endeavoured to determine whether van Bogaert-Bertrand's disease is to be considered as congenital or acquired. The anatomical findings in 3 cases together with the descriptions of other authors lead us to the following conclusions: -that the spongiform changes may be due to an osmolar disequilibrium in which the ATPase-Na/K relation with mitochondrial abnormalities is yet unclear. -that the constant finding of Alzheimer type II cells is certainly an indication of intra-astrocytic malfunction. -that the oedema blocks both myelin synthesis and its coiling into lamellae. Case 1, which showed a long survival compared to others described (about 4 years), enabled us to study terminal lesions. Sub-cortical zones, in both cerebrum and cerebellum, contained neither myelin nor spongiform cavities, but, on the other hand, showed a compact glio-fibrillosis with large vesicles and oligodendroglia of increased density. We have interpreted these lesions, progressively replaced by spongiosis deeper in the cortex, as evidence of retracted scar tissue. Differences found between cerebral weights seem to confirm this hypothesis.
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PMID:[Hereditary spongiform dystrophy in young children (Canavan: van Bogaert-Bertrand)]. 127 Oct 80

Magnesium is an essential cofactor for many enzymatic reactions, especially those involved in energy metabolism. Deficits of magnesium are prevalent due to inadequate intake or malabsorption and due to the renal loss of magnesium that occurs in certain disease states (alcoholism, diabetes) and with drug therapy (diuretics, aminoglycosides, cisplatin, digoxin, cyclosporin, amphotericin B). Protracted deficits of magnesium in humans and animals result in neurological disturbances, including hyperexcitability, convulsions and various psychiatric symptoms ranging from apathy to psychosis, some of which can be reversed with magnesium supplementation, others requiring correction of the dysregulation mechanism. Although the role of magnesium in neuronal function is not completely understood, a lowering of CSF or brain magnesium can induce epileptiform activity and there is an association between decreased CSF magnesium and the development of seizures. CSF concentrations of magnesium are normally higher than magnesium plasma ultrafiltrate (diffusible) concentrations due to the active transport of magnesium across the blood-brain barrier. Under conditions of magnesium deficiency, CSF concentrations decline, although this decline lags behind and is less pronounced than the changes observed in plasma magnesium concentrations. Decreases in CSF magnesium concentrations correlate with the alterations observed in extracellular brain magnesium concentrations in animals following the dietary deprivation of magnesium. CSF magnesium concentrations can readily be repleted following magnesium supplementation, although high dose magnesium therapy, such as that used in the treatment of convulsions in eclampsia, will only increase CSF magnesium concentrations to a very limited degree (approximately 11-18 per cent) above physiological concentrations. Greater increases in CSF magnesium may occur in neonates since neonatal swine, following treatment with magnesium, have CSF magnesium concentrations that are similar to their plasma concentrations. There has been a recent resurgence of interest in magnesium deficiency and its neurological consequences due to the finding that magnesium, at physiological concentrations, blocks N-methyl-D-aspartate (NMDA) receptors in neurones. NMDA receptors are normally activated by glutamate and/or aspartate which represent the principal neurotransmitters for excitatory synaptic transmission in vertebrate CNS. Magnesium deficiency produces epileptiform activity in the CNS which can be blocked by NMDA receptor antagonists. Other mechanisms, including alterations in Na+/K(+)-ATPase activity, cAMP/cGMP concentrations and calcium currents in pre- and postsynaptic membranes, may also be at least partially responsible for the neuronal effects associated with low brain magnesium. Further studies are necessary to increase our understanding of the neurological implications of magnesium deficit in the central nervous system.
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PMID:Brain and CSF magnesium concentrations during magnesium deficit in animals and humans: neurological symptoms. 129 67


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