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)

Myosin from rabbit stomach was highly purified by ammonium sulfate fractionation in the presence of ATP and MgCl2, ultracentrifugation and Sepharose 4B chromatography. The myosin composed of one heavy and two light chains as determined by SDS-gel electrophoresis. The molecular weights of the light chains were the same as those of gizzard myosin, about 20,000 and 17,000, respectively. The pH-activity curve and the KCl concentration dependency of Ca-ATPase of the stomach myosin were similar to those of other smooth muscle myosins. The stomach myosin was more resistant to pepsin digestion than skeletal myosin. Other proteolytic enzymes, trypsin, chymotrypsin, papain, and nagarse, digested the myosin in the same way as skeletal myosin.
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PMID:Purification and some properties of rabbit stomach myosin. 1 37

Pb2+-stimulated phosphorylation of Electrophorus electricus electroplax (Na+ + K+)-adenosine triphosphatase is prevented by stoichiometric quantities of 2,3-dimercaptopropanol. The chelator in the same low concentrations does not block Na+-dependent phosphorylation. Both Pb2+-and Na+-dependent phosphorylation reactions show the same dependence on MgCl2. Phosphorylation in the presence of both Na+ and Pb2+ is cumulative suggesting that Pb2+ and Na+ bind at separate, independent sites. The enthalpy change due to binding of Pb2+ is about -1.76 kcal/mol. 32P-phosphopeptides obtained from pronase or pepsin digests of Pb2+-and Na+-dependent phosphoproteins are electrophoretically identical. Pb2+ does not stimulate but does inhibit ATP-ADP exchange activity under the conditions in which this activity is stimulated by Na+. Since the phosphorylation sites are identical, it is concluded that the differences in reactivity of the Na+- and Pb2+-phosphoenzymes are due to different conformational changes produced by binding of Na+ and Pb2+. The Pb2+-sensitive conformation is critical for Na+ specificity of phosphorylation, reversibility of phosphorylation, and for phosphatase activity but not for acceptor site phosphorylation by ATP. These findings have implications for enzyme reaction models.
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PMID:Characteristics of lead ion-stimulated phosphorylation of Electrophorus electricus electroplax (Na+ + K+)-adenosine triphosphatase and inhibition of ATP-ADP exchange. 21 19

Proton pump inhibitor is a compound recently applied for the treatment of peptic ulcers for its strong action to inhibit the gastric acid secretion. It works through inhibition of H+, K(+)-ATPase, so called proton pump, on the luminal surface of secretory canaliculi in the parietal cells, showing remarkable characteristics in the inhibition of gastric acid secretion; e.g., the long-acting and complete inhibition. At neutral pH, the unionized form of this compound as a weak base is lipophilic, and passes through the cell membrane to accumulate as the ionized form in an acidic environment in the secretory canaliculi of parietal cells, where it is transformed to an active molecule which binds covalently to the active site of H+, K(+)-ATPase, forming a highly stable complex. The long-acting and complete inhibition of gastric acid secretion by this compound is derived from this physico-chemical nature. The above characteristics of the proton pump inhibitor have been confirmed with the basal, stimulated and nocturnal gastric acid secretion and the 24-hour intragastric pH of healthy volunteers by several investigators prior to its nation-wide clinical trial in Japan. On the other hand, the increased endocrine and exocrine secretion, such as pepsin secretion and gastrin release, and the increased turnover of gastrointestinal endocrine cells by this compound have been reported in animal models, probably due to its accumulation in the acidic environment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Characteristic features of proton pump inhibitors in the inhibition of gastric acid secretion: long-acting and complete inhibition]. 131 89

The gastric duodenal mucosa normally is protected from the damaging effects of gastric acid and pepsin by ill-defined mechanisms. Ulcers may arise when there is an imbalance between the aggressive and defensive factors that renders the mucosa susceptible to damage. A variety of factors have been identified that may favor the development of peptic ulcers, but no single pathophysiologic defect applies in all ulcer patients. In duodenal ulcers, gastric acid hypersecretion is observed in as many as one third of patients; however, most patients with duodenal ulcers secrete normal amounts of gastric acid. Decreased mucosal bicarbonate secretion may be important in at least some duodenal ulcer patients. Use of NSAIDs may cause either gastric or duodenal ulcers, probably through the inhibition of mucosal prostaglandin synthesis and disruption of mucosal defenses. Finally, a recently identified bacterium, H. pylori, causes a chronic gastritis that is found in the overwhelming majority of patients with duodenal ulcers and non-NSAID-associated gastric ulcers. This bacterium may play a pivotal role in ulcer pathogenesis and, especially, in ulcer recurrences. A number of drugs of proved efficacy are available for the treatment of acute duodenal and gastric ulcers. The H2 receptor antagonists administered once daily remain the mainstay of ulcer therapy because of their efficacy, ease of use, and excellent safety profile. More thorough and long-lasting acid inhibition is afforded by the H+/K(+)-ATPase inhibitor omeprazole. This agent also promotes more rapid ulcer healing, but in most patients, this minor advantage may not justify the higher cost. It is not known whether more rapid healing will translate into lower ulcer complication rates. Until further data are available, this drug may be preferable in patients with large or complicated ulcers. In patients with refractory ulcers, omeprazole is clearly superior to other available agents. Agents that promote mucosal defense mechanisms are becoming increasingly popular in the treatment of duodenal ulcers but have undergone less testing than in gastric ulcers. Sucralfate 1 g four times daily is equivalent to H2 antagonists in the treatment of duodenal ulcers and, probably, gastric ulcers. Its requirement for multiple daily doses makes it somewhat less attractive at present to most patients. Low- to medium-dose Al-containing antacids are inexpensive and efficacious in duodenal ulcer therapy. They should remain as therapeutic options for the compliant patient in whom cost considerations are important. Colloidal bismuth subcitrate 120 mg four times a day is comparable to other agents in the acute treatment of duodenal ulcers and likely gastric ulcers.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Medical therapy of peptic ulcer disease. 134 60

Nascent synthesis and accumulation of germin and its mRNA mark the onset of renewed growth when wheat embryos are germinated in water. Germin is a water-soluble, pepsin-resistant protein that is not found in immature embryos, or in mature embryos before their germination. An antiserum was raised by injecting rabbits with germin that was freed of other proteins by pepsinization and gel filtration. The antiserum has been used to detect, in extracts of mature embryos from dry, ungerminated wheat grains, a protein that is antigenically related to germin. The antigenically related protein has been named pseudogermin. Pseudogermin accumulates, maximally, between 20-25-days postanthesis, then declines appreciably in amount by 30-days postanthesis, in soluble extracts of immature embryos from several wheat varieties. The antiserum was also used to identify germin and pseudogermin among the proteins extracted from cell walls and to bind immunogold to cell walls preparatory to visualizing freeze-cleaved embryos by scanning electron microscopy. Wall-associated germin accounts for about 40% of the total germin in germinating wheat embryos. Appearance of germin in the apoplast is the most conspicuous germination-related change in the distribution of cell-wall proteins. It seems that germin may act at the level of the apoplast and that pseudogermin may subsume the role of germin at low water potentials during embryogenesis. The N-terminal eicosapeptide sequences in germin and pseudogermin are very similar but SDS/PAGE analysis detects discrete differences between the mobilities of their constituent monomers as well as gross differences between the stabilities of the parent oligomers. Like germin, pseudogermin is a water-soluble, pepsin-resistant protein, but pseudogermin has unprecedented disulphide-independent thermostability properties that have never been previously reported for a water-soluble oligomeric protein. Polysaccharides that co-purify with otherwise pure specimens of germin (and pseudogermin) have been isolated for analysis and shown to be highly substituted glucuronogalactoarabinoxylans. The possible biological significance of selective and tenacious association between germin and glucuronogalactoarabinoxylans is discussed in relation to cell expansion during embryogenic and germinative development of wheat, as are some peculiarities of amino-acid sequence that suggest a possible relation between germin and a proton-specific ion pump: gastric ATPase.
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PMID:Germin isoforms are discrete temporal markers of wheat development. Pseudogermin is a uniquely thermostable water-soluble oligomeric protein in ungerminated embryos and like germin in germinated embryos, it is incorporated into cell walls. 142 3

It is generally accepted that ulcer pathogenesis is mainly mediated by an imbalance between aggressive factors as gastric acid and pepsin, and obviously genetically determined defects in protection mechanisms of the gastric and duodenal mucosa. Since at present it is not possible to substitute these defects properly by pharmacological measures, the modern ulcer therapy aims to a distinct acid reduction as the main and most successful therapeutic principle. Recent studies show a direct correlation between the effectiveness and the acid reducing potency of a given anti-ulcer drug, assessed by pH above 3 over time. By long term treatment using H2-blockers and most recently the ATPase inhibitor Omeprazole it is now possible to reduce drastically the relapse rates of gastrointestinal ulcers and to improve significantly quality of life. An effective prophylaxis in duodenal ulcer can also be achieved by combination therapy with bismuth plus antibiotics or with omeprazole plus antibiotics. Even ulcers induced by nonsteroidal-antirheumatic drugs or acetylsalicylate can be adequately treated and prevented by acid reducing drugs. The present article includes pathophysiological and pharmacological backgrounds of medical ulcer therapy as well as guidelines for indication and mode of application of the different antiulcer drugs concerning short and long term treatment.
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PMID:[Current therapy of ulcer disease]. 150 68

The occurrence of auto-antibodies in patients with the autoimmune disease pernicious anaemia and in patients with active duodenal ulcers was investigated. In order to characterize antigenic structures, various cellular and subcellular fractions were prepared from pig gastric mucosa and from a homogenate of duodenal mucosa. By means of an enzyme-linked immunosorbent assay and immunoblotting, both the H+,K(+)-ATPase and pepsinogen/pepsin were shown to constitute the major antigens. All of the seven pernicious-anaemia sera that were tested contained auto-antibodies against both antigens, and the epitopes of the H+,K(+)-ATPase were shown to be localized on its cytoplasmic face. In 75% (18/24) of the sera from patients with duodenal ulcers, auto-antibodies were detected when using purified antigens. Six sera reacted with H+,K(+)-ATPase and twelve reacted with pepsinogen, one reacted with both antigens, and four sera reacted with the duodenal mucosal antigen. The occurrence of auto-antibodies indicates that there is a mucosal lesion and that immunological factors may be involved in the pathogenesis of the disease in some patients.
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PMID:The occurrence of auto-antibodies in patients with gastro-duodenal lesions. 169 83

Spontaneous remission of gastric acid hypersecretion in the Zollinger-Ellison syndrome occurs rarely. This study shows the development of gastric secretory mucosal atrophy resulting in achlorhydria and loss of pepsin secretion in a 63-year-old woman with the Zollinger-Ellison syndrome. Reduced secretion began soon after starting treatment with omeprazole, and achlorhydria became complete 6 months later. The patient remains well with normal endoscopy results and is achlorhydric 4 years after the start of treatment and 34 months after stopping omeprazole. She was not colonized with Helicobacter pylori until 36 months after developing achlorhydria. Serum gastrin has increased from 1000 to between 5000 and 12,500 ng/L (pg/mL), was not suppressible by gastric acidification, and was not associated with G-cell hyperplasia. She also has a normal Schilling test and normal immunoglobulins, and lacks antibodies to parietal cells or H+, K(+)-ATPase. Moderate enterochromaffinlike cell hyperplasia is apparent for the first time on the latest biopsy sample.
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PMID:Development of sustained achlorhydria in a patient with the Zollinger-Ellison syndrome treated with omeprazole. 179 40

Trifluoperazine (TFP) 5, 10, 20 mg.kg-1 ig inhibited the formation of gastric ulcers induced by pyloric ligation, stress and indomethacin in rats and showed dose-effect dependence. TFP 10, 20 mg.kg-1 ig depressed the secretion of gastric juice, acid, and pepsin, but TFP 5, 10, 20 mg.kg-1 ig had no influence on the pepsin activity. TFP 20 mg.kg-1 ig inhibited the gastric H+, K(+)-ATPase activity of both stress and indomethacin ulcers in rats in vivo, and the gastric H+, K(+)-ATPase activity was also inhibited by TFP 50 mumol.L-1 in vitro. The results suggested that the inhibition of gastric H+, K(+)-ATPase activity and gastric secretion might be related to the antiulcer mechanism of TFP.
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PMID:[Antiulcer action and mechanism of trifluoperazine in rat stomach]. 181 2

Sixty-seven invited participants involved in the development, evaluation, and use of therapies for acid-peptic disorders participated in a meeting to discuss the scientific basis for healing actions of ulcer drugs and the prospects for future developments ("Realities of Mucosal Protection in the Upper Gastrointestinal Tract," Lausanne, Switzerland, November 8-10, 1987). Eighty-one key statements were prepared and subsequently analyzed on the basis of a voting system. Of the 45 statements that dealt with existing therapies, only 3 statements showed positive consensus (agreement of two-thirds or more of voters) about mechanisms of ulcer healing. Participants agreed that both (1) hydrogen/potassium adenosine triphosphatase inhibitors and (2) histamine H2 antagonists healed ulcers solely by acid inhibition, and (3) that sucralfate works by topical action. Substantial uncertainty about the mechanisms by which bismuth compounds and antacids heal ulcers was noted as well as their wide range of effects. The mechanism of ulcer healing by prostaglandins and the clinical relevance of antiulcer effects of drugs demonstrated in acute studies with animals were also controversial. There was greater agreement among participants about unexplored drug effects that might produce ulcer healing. Of the 36 such mechanisms surveyed, the most support went to therapies aimed at enhancement of mucosal blood flow, epithelial restitution, and mucosal alkaline secretion or inhibition of luminal pepsin activity. The diversity of opinions among participants suggests a high level of empiricism in the development of ulcer healing drugs apart from those that inhibit acid secretion. This empiricism probably arises from inadequate understanding of processes of mucosal injury and repair.
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PMID:Current and future drugs for acid-peptic disease: a plethora of opinions on possible mechanisms of action. 208 36


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