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:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experiments over the past decade have revealed a third component in the autonomic nervous system which is neither adrenergic nor cholinergic. These nerves are strongly represented in the gastrointestinal tract of a wide range of vertebrate species and have also been identified in lung, trachea, retractor penis, bladder, oesophagus, eye, seminal vesicle and in some parts of the cardiovascular system and brain. Evidence has been presented that the principal active substance released by these nerves in the gut is a purine nucleotide, probably ATP, and they have therefore been termed 'purinergic'. The evidence includes: (1) synthesis and storage of ATP in nerves; (2) release of ATP from the nerves when they are stimulated; (3) mimicry by exogenously applied ATP of the action of nerve-released transmitter; (4) the presence of Mg2+-activated ATPase, 5'-nucleotidase and adenosine deaminase, enzymes which inactivate ATP; (5) the similar blocking and potentiating effects produced by drugs on the responses to exogenously applied ATP and nerve stimulation. A tentative model for the synthesis, storage, release and inactivation of ATP during purinergic nerve transmission is proposed. Some properties of purinergic receptors are described.
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PMID:The purinergic nerve hypothesis. 2 31

The Ca2+-pumping ATPase from human erythrocyte membranes, purified nearly to homogeneity (Niggli, V., Penniston, J. T., and Carafoli, E. (1979) J. Biol. Chem. 254, 9955-9958), can be reconstituted into phospholipid vesicles. The purified and the reconstituted forms of the enzyme displayed the properties expected of the intact Ca2+ pump; they had an appropriate (Ca2+-Mg2+)-ATPase activity which displayed a relatively low affinity for Ca2+. Added calmodulin increased both the maximum rate and the affinity for Ca2+ of the enzyme. Mg2+ alone caused no significant ATP hydrolysis in the purified enzyme, indicating that the Mg2+-ATPase is a separate enzyme. Vesicles of the reconstituted enzyme accumulated Ca2+ with a ratio of Ca2+ accumulated to ATP hydrolyzed of approximately 1. Ca2+ accumulation and ATPase of the reconstituted enzyme were inhibited concurrently by vanadate ion, with a K 1/2 for inhibition which was indistinguishable from that observed for the (Ca2+-Mg2+)-ATPase in whole erythrocyte ghosts. While the above properties were all consistent with those observed for the (Ca2+-Mg2+)-ATPase in whole erythrocyte ghosts, the purified enzyme displayed an unexpected response to acidic phospholipids. Enzyme reconstituted with or prepared in phosphatidylserine acted as if calmodulin were already present, and added calmodulin caused no effect beyond that due to phosphatidylserine. This mimicry of the calmodulin effect by acidic phospholipids is similar to that reported for cyclic nucleotide phosphodiesterase (Wolff, D. J., and Brostrom, C. O. (1976) Arch. Biochem. Biophys., 173, 720-723).
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PMID:Purified (Ca2+-Mg2+)-ATPase of the erythrocyte membrane. Reconstitution and effect of calmodulin and phospholipids. 610 53

Based on clinical studies, a negative association between Helicobacter pylori and autoimmune corpus gastritis is described. In the present investigation of an unselected population of 1461 adults we can state, however, that there exists a relationship between H. pylori infection and the development of gastric corpus autoimmunity. As confirmation for the gastric autoantibody development through molecular mimicry, a high homology (72% in 25 amino acid overlap) between the beta subunit of H. pylori urease and that of H + K + ATPase, the gastric parietal cell autoantigen, was revealed.
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PMID:Association of Helicobacter pylori and gastric autoimmunity: a population-based study. 759 5

Sublethal concentrations of hydroperoxides (H2O2 or tert-butylhydroperoxide) produce a dual effect upon the respiratory burst of rat alveolar macrophages in which low concentrations (< 50 microM) enhance and higher concentrations (> 50 microM) produce inhibition (J. K. Murphy, et al., Free Radical. Biol. Med. 18, 37-45, 1995). These effects correlate with transient versus sustained elevation of [Ca2+]i caused by exposure to hydroperoxides prior to stimulation of the respiratory burst. In the present study changes in [Ca2+]i caused by exposure to sublethal levels of hydroperoxide were buffered by incubating macrophages with the acetoxy-methyl ester of BAPTA, an intracellular Ca2+ chelator. The enhancement of the phorbol ester-stimulated respiratory burst by tBOOH was abolished by BAPTA, while the inhibition was attenuated. Thus, the modulation by tBOOH appears to be largely dependent upon the changes in [Ca2+]i. Receptor mediated stimulation of the respiratory burst (ADP stimulation) involves release of Ca2+ from the inositol-1,4,5-triphosphate (IP3)-sensitive pool in the endoplasmic reticulum. Comparisons were made of the effects of thapsigargin (TG), an endoplasmic reticulum Ca-ATPase inhibitor, with tBOOH on release of intracellular Ca2+ and the respiratory burst. Treatment with TG did not affect changes in [Ca2+]i caused by tBOOH or vice versa. Although TG decreased the ADP-stimulated respiratory burst, it had no effect upon tBOOH modulation. Thus, the effect of tBOOH upon the respiratory burst is dependent upon the release of Ca2+ and the release of Ca2+ occurs from a non-IP3-dependent pool. This aberrant mimicry of normal signal transduction underlies oxidative modulation of the respiratory burst.
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PMID:Modulation of the rat alveolar macrophage respiratory burst by hydroperoxides is calcium dependent. 857 66

Helicobacter pylori is involved in gastritis, gastric and duodenal ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. Earlier studies already suggested a role for autoimmune phenomena in H. pylori-linked disease. We now report that lipopolysaccharides (LPS) of H. pylori express Lewis y, Lewis x, and H type I blood group structures similar to those commonly occurring in gastric mucosa. Immunization of mice and rabbits with H. pylori cells or purified LPS induced an anti-Lewis x or y or anti-H type I response, yielding antibodies that bound human and murine gastric glandular tissue, granulocytes, adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma cells. Experimental oral infections in mice or natural infection in humans yielded anti-Lewis antibodies also. The beta chain of gastric (H+,K+)-ATPase, the parietal cell proton pump involved in acid secretion, contained Lewis y epitopes; gastric mucin contained Lewis x and y antigenic determinants. Growth in mice of a hybridoma that secretes H. pylori-induced anti-Lewis y monoclonal antibodies resulted in histopathological evidence of gastritis, which indicates a direct pathogenic role for anti-Lewis antibodies. In conclusion, our observations demonstrate that molecular mimicry between H. pylori LPS and the host, based on Lewis antigens, and provide understanding of an autoimmune mechanism for H. pylori-associated type B gastritis.
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PMID:Potential role of molecular mimicry between Helicobacter pylori lipopolysaccharide and host Lewis blood group antigens in autoimmunity. 867 4

The cellular activity of several regulatory and signal transduction proteins, which depend on the Hsp90 molecular chaperone for folding, is markedly decreased by geldanamycin and by radicicol (monorden). We now show that these unrelated compounds both bind to the N-terminal ATP/ADP-binding domain of Hsp90, with radicicol displaying nanomolar affinity, and both inhibit the inherent ATPase activity of Hsp90 which is essential for its function in vivo. Crystal structure determinations of Hsp90 N-terminal domain complexes with geldanamycin and radicicol identify key aspects of their nucleotide mimicry and suggest a rational basis for the design of novel antichaperone drugs.
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PMID:Structural basis for inhibition of the Hsp90 molecular chaperone by the antitumor antibiotics radicicol and geldanamycin. 992 31

Helicobacter pylori lipopolysacchararide expresses Lewis x and/or y blood group antigens in mimicry with human gastric epithelial cells. Mimicry may have two diverging roles in pathogenesis. Infection may break tolerance and anti-Lewis antibodies may be induced that bind to gastric mucosa and cause damage. Secondly, mimicry may cause "invisibility" of the pathogen to the host, thus aiding persistence of infection. We demonstrate that Helicobacter pylori induces autoantibodies during infection. In orally infected pigs, these were specific for Lewis epitopes present on parietal cell H+K(+)-ATPase. In contrast, in infected patients the autoantibodies were directed to protein epitopes of H+K(+)-ATPase not induced through mimicry.
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PMID:Helicobacter pylori LPS: molecular mimicry with the host and role in autoimmunity. 1007 49

Recent studies suggest a significant association of Helicobacter pylori (H.p.) gastritis and antigastric autoimmunity. Sera of H.p. infected patients exhibit antigastric autoantibodies with high prevalence (over 50 percent of the cases) and with antiluminal and/or anticanalicular binding patterns on gastric mucosa. Models for the pathogenesis of this H.p. associated autoimmunity are antigenic mimicry or Th 1-induced expression of MHC class II and costimulatory molecules on gastric epithelial cells. The anticanalicular autoantibodies binding to gastric parietal cells show fine specificities for the alpha- and for the beta-subunit of the gastric H, K-ATPase, which correspond to the findings in classical autoimmune gastritis. They are significantly correlated with higher grades of corpus gastritis as well as morphologic and functional glandular atrophy of the corpus. The development of this antigastric autoimmunity apparently is a relevant pathogenic factor of the host reaction and might be crucial for the different types and outcomes of H.p. gastritis.
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PMID:[Helicobacter pylori infections and autoimmunity: the interplay in the pathogenesis of gastritis]. 1071 95

Recent studies report a significant association between Helicobacter pylori gastritis and autoimmune reaction. Antigastric autoantibodies are detectable in about 30% of H. pylori infected patients. Two major in situ binding sites have been found: first, at the luminal membrane of the foveolar epithelium in antrum and corpus mucosa and, second, at canalicular membranes within parietal cells in the corpus mucosa. The presence of latter type of autoantibodies is correlated with histological and clinical parameters of corpus mucosa atrophy. The gastric H+/K(+)-ATPase, which is already known as an autoantigen in classic autoimmune gastritis, also represents a major target in atrophic H. pylori gastritis. According to recent data molecular mimicry between H. pylori and the host does not play a pathogenic role in the formation these autoantibodies. In conclusion, antigastric autoimmunity represents a relevant host factor which contributes to the final outcome of H. pylori gastritis.
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PMID:[Helicobacter pylori and antigastric autoimmunity]. 1122 41

Autoimmune gastritis and Helicobacter pylori-associated gastric atrophy develop through similar mechanisms involving the proton pump H+,K+-adenosine triphosphatase as autoantigen. Here, we report that H. pylori-infected patients with gastric autoimmunity harbor in vivo-activated gastric CD4+ T cells that recognize both H+, K+-adenosine triphosphatase and H. pylori antigens. We characterized the submolecular specificity of such gastric T cells and identified cross-reactive epitopes from nine H. pylori proteins. Cross-reactive H. pylori peptides induced T cell proliferation and expression of T helper type 1 functions. We suggest that in genetically susceptible individuals, H. pylori infection can activate cross-reactive gastric T cells leading to gastric autoimmunity via molecular mimicry.
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PMID:Molecular mimicry between Helicobacter pylori antigens and H+, K+ --adenosine triphosphatase in human gastric autoimmunity. 1456 77


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