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)

Non specific immunity in human rheumatoid synovium: histochemical and immunohistological analysis. Enzymatic activities and monocyte-specific membrane antigens were looked for on frozen sections from 25 synovial membrane samples from patients with rheumatoid arthritis. Classical histochemical reactions were used to identify non specific esterases, alkaline and acid phosphatases, ATPase and peroxidase. Indirect immunofluorescence was performed with a series of monoclonal antibodies to monocyte membrane antigens and HLA class II molecules. Technical pitfalls were successfully overcome, and specific labelings demonstrated the variety and heterogeneity of these markers among synovial cells and vascular endothelia. Reported data indicated that such a panel of investigations is useful to better define the non-specific immunological phenomenons which take place in this active pathological tissue. They suggest that numerous metabolic activities concur to sustain chronic inflammation.
Rev Rhum Mal Osteoartic 1986 Dec
PMID:[Mononuclear phagocytic cells in human rheumatoid synovial membrane. Histochemical and immunohistological study]. 354 8

Semi-purified dog kidney Na+-K+-ATPase was cross-linked with ovalbumin. This immobilized enzyme was able to hydrolyse ATP and this hydrolysis was ouabain-sensitive. It was then used in batch wise affinity chromatography for the detection of endogenous Na+-K+-ATPase inhibitor in human plasma and urine. Ammonium acetate 1 mM washed off the endogenous Na+-K+-ATPase inhibitor from the immobilized enzyme. The inhibitory activity of the eluate from hypertensive plasma was significantly higher (p less than 0.0025, n = 6) than that of normotensive plasma. Similar results were obtained (n = 3) from human urine eluates during salt loading as compared to control urine.
Arch Mal Coeur Vaiss 1984 Oct
PMID:[Affinity chromatographic study of the changes in the endogenous Na+-K+-ATPase inhibitor during sodium loading in man]. 609 36

Active Na+ and Ca2+ transports by sarcolemmal vesicles from young spontaneously hypertensive rats (SHR) and their normotensive controls (WKY) were compared. The effects of the calmodulin and the calcium antagonist nifedipine on Ca2+ binding ATP-dependent accumulation of Ca2+ were studied at free Ca2+ concentrations of 2.10(-8)M and 4.10(-7)M. 2.10(-7)M calmodulin stimulated Ca2+ binding to SHR membranes up to a level equivalent to that in WKY, whereas it enhanced active Ca2+ transport more in WKY than in SHR, thus suppressing the difference between the two substrains. At a 2.10(-8)M free Ca2+ concentration low concentrations of nifedipine (10(-7) to 10(-6)M) induced an increases in ATP-dependent Ca2+ transport by SHR vesicles. Inhibition of NA+, K+-adenosine triphosphatase activity by ouabain was also studied. Na+, K+ATPase activity in SHR membranes was double that in membranes from WKY (22.1 +/- 2.8 v.s. 11.3 +/- 1.1. mumole Pi/h/mg protein). These differences, observed on 3 week-old rats, before a significant rise blood pressure, may reflect genetic characteristics of these hypertensive-prone rats.
Arch Mal Coeur Vaiss 1984 Oct
PMID:[Active calcium and sodium transport by cardiac plasma membranes in the genetically hypertensive rat]. 609 37

The presence of a circulating Na+ pump inhibitor has been assessed in 112 subjects by studying the effects of deproteinized plasma on ouabain binding to erythrocytes and/or inhibition of Na+-K+-ATPase activity. High levels of an inhibitor possessing some digitalis-like properties, were associated with essential hypertension, hypertensive heredity, treatment of hypertension with beta-blocking agents and high sodium intake. Low levels were found in hypertensives on diuretics, patients with chronic renal failure and normotensive controls. These observations are consistent with a possible role of this circulating inhibitor in the control of sodium balance and in hypertension.
Arch Mal Coeur Vaiss 1984 Oct
PMID:[Circulating inhibitor of the Na+-K+ pump in essential hypertension. Physiological and pharmacological variations]. 609 38

Electron transport particles and purified H+-ATPase (F1-F0) vesicles from beef heart mitochondria have been treated with two classes of thiol reagent, viz. membrane-impermeable organomercurials and a homologous series of N-polymethylene carboxymaleimides (Mal-(CH2)x-COOH or AMx). The effect of such treatment on ATP-driven reactions (ATP-Pi exchange and proton translocation) has been examined and compared to the effects on rates of ATP hydrolysis. The organomercurials inhibited ATP-Pi exchange and one of them (p-chloromercuribenzoate) inhibited ATPase activity. Of the maleimide series (AMx), AM10 and AM11 inhibited both ATP-Pi exchange and ATP-driven membrane potential, but not ATPase activity. The other members of the series were essentially inactive. N-Ethylmaleimide was intermediate in its efficacy. Passive H+ conductance through the membrane sector F0 was 50% blocked by AM10, slightly blocked by AM2 and N-ethylmaleimide, and unaffected by the other members of the AMx series. The data imply that one -SH near the membrane surface and one -SH about 12 A from the surface are functional in proton translocation through the H+-ATPase.
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PMID:Environment of the sulfhydryl groups in bovine heart mitochondrial H+-ATPase. 610 Mar 75

Treatment of demembranated sea-urchin sperm for 1-2 min with 10 microM-N-ethylmaleimide (Mal-NEt) at pH 8.0 prior to reactivation with 1 mM-ATP causes the asymmetry of the flagellar waveform to become desensitized to the presence or absence of Ca2+ in the reactivating medium. In such sperm, changes in concentration of free Ca2+ between 10(-7) M and 10(-3) M have no effect on the asymmetry of the waveforms as measured by the turning rate of the sperm in radians per beat cycle, while the beat frequency and the propulsive efficiency of the waves remain unchanged from the values observed in control preparations not treated with MalNEt. A somewhat more prolonged treatment with MalNEt causes a progressive decrease in the bend angles of the flagellar waves, while the beat frequency and the wavelength still remain largely unchanged. Further extension of the treatment with MalNEt causes complete loss of motility. Little ATP-induced sliding of the doublet tubules is observed upon treatment with trypsin of sperm flagella that have been rendered non-motile with MalNEt. However, the preparations of solubilized dynein 1 obtained by 0.6 M-NaCl extraction of axonemes treated with MalNEt appear almost identical to those obtained from untreated axonemes, both in terms of the amount solubilized and in the specific ATPase activities of their latent and Triton-activated forms. These preparations also appear capable of restoring much of the beat frequency of dynein-1-depleted flagella. These results suggest that the observed desensitization to Ca2+ and decrease in bend angle result from the reaction of MalNEt with axonemal polypeptides that are not part of the dynein 1 particle extracted with 0.6 M-NaCl. The rate of ATP hydrolysis by demembranated sperm rendered non-motile with MalNEt remains relatively high, and it decreases about 50% when the flagella are broken by brief homogenization. This 'homogenizer-sensitive' ATPase activity appears to be derived from some flagellar regulatory mechanism, which controls the ATPase activity of intact non-motile axonemes.
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PMID:Modification of flagellar waveform and adenosine triphosphatase activity in reactivated sea-urchin sperm treated with N-ethylmaleimide. 622 31

The fluorescent maleimide derivatives, 2-(4'-maleimidylanilino)naphthalene 6-sulfonic acid (Mal-ANS) and N-(1-pyrene)-maleimide (Mal-pyrene), both alkylate sulfhydryl groups on the alpha subunit of the (Na,K)-ATPase to inhibit (Na,K)-ATPase and p-nitrophenyl phosphatase activities and phosphoenzyme formation. Reaction of the enzyme with Mal-pyrene, but not with Mal-ANS, also inhibits MgPi- and Mg.ATP.Na-supported [3H]ouabain-binding to the enzyme. Mal-pyrene and Mal-ANS react, in part, with different sulfhydryl groups on the enzyme protein. On the average, the sulfhydryl groups which react with Mal-pyrene are located in a more shielded or hydrophobic environment than are those which react with Mal-ANS. It is the reaction of Mal-pyrene with sulfhydryl groups, which are not accessible to Mal-ANS, that results in the decreased [3H]ouabain-binding capacity of the (Na,K)-ATPase. The results indicate that phosphorylation of (Na,K)-ATPase is not required for Mg.ATP.Na-stimulated ouabain binding, and suggest that the ATP and sodium sites which modulate the interaction of ouabain with the (Na,K)-ATPase may be different from those which promote phosphorylation.
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PMID:Reaction of (Na,K)-ATPase with fluorescent maleimide derivatives. Probes for studying ATP site(s) function. 630 Jan 9

Increasing evidence indicates that sodium ingestion in the face of an inability to excrete it normally causes hypertension by releasing a humoral pressor substance. This substance, which is probably the putative natriuretic hormone, inhibits Na+-K+-ATPase and thereby increases cardiac contractility and blood vessel tone. Potassium may be antihypertensive in part by virtue of its ability to stimulate Na+-K+-ATPase in the vascular smooth muscle cells and in adrenergic nerve endings, thereby causing vasodilation.
Arch Mal Coeur Vaiss 1984 Apr
PMID:[The sodium-potassium pump in hypertension. Mechanisms of action of potassium]. 632 19

Much experimental and clinical evidence points to the fact that increased intracellular Na+ concentration could play an important pathogenic role in hypertension, especially where cells of excitable tissues are concerned. Active extrusion of Na+ (from the cells to the extracellular space) depends mainly on the activity of the system of membrane transport known as the Na+ pump. The extrusion of Na+ occurs in exchange for K+ and the activity of the pump depends on the enzyme Na+-K+-ATPase. The Na+ pump is inhibited by cardiotonic glycosides such as digitalis and ouabain . The results obtained in our laboratory suggest that the activity of the Na+ pump is controlled by an endogenic system acting in a similar manner to ouabain and digitalis. Experimental and clinical studies show: -- that the administration of Na+ increases the inhibitor effect both in urine and plasma; -- that the inhibitor is increased in about 50 p. 100 of patients with essential hypertension; -- that this increase seems to depend on familial or genetic factors. The biochemical identification of this endogenic inhibitor is now under way; it has a small molecular weight (less than 3000), is thermostable and anionic. This factor could have both a regulating role on Na+ turnover and a pathological role in hypertension. Its activity comes into competition cations also capable of inhibiting the Na+ pump, including K+.
Arch Mal Coeur Vaiss 1984 Apr
PMID:[Essential arterial hypertension, cellular intolerance to sodium]. 632 20

The aim of this introductory paper is to describe the movements of the two major cations of the myocardial intracellular compartment, potassium and magnesium. The role of the potassium ion, which participates in an active manner in the development of transmembrane potential changes during the cardiac cycle, is treated in terms of membrane conductance, driving force and active transport (Na-K-ATPase). The magnesium ion, of which role mainly concerns intracellular metabolic activity and interactions on the membrane exchanges of other ions is considered under three main aspects: its action on Na-K-ATPase and its effects on the electrophysiological properties and contractile activity of the cardiac fibres. Disturbances of the exchanges of these two cations during myocardial ischaemia and their importance in the field of cardioplegia are briefly discussed.
Arch Mal Coeur Vaiss 1984 Apr
PMID:[Potassium and magnesium in the myocardial cell: general data]. 642 67


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