Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ectodermal cells of the two- and three-germ layer-thick mouse egg-cylinders are considered to be the progenitors of embryonal carcinoma cells in embryo-derived teratocarcinomas. In an attempt to find differences between the tumor cells and equivalent embryonic cells, we have studied the electron microscopic cytochemical localization of alkaline phosphatase, 5'-nucleotidase, and Mg2+-activated adenosine triphosphatase (ATPase) in embryo-derived teratocarcinomas and mouse egg-cylinders. Alkaline phosphatase was detected in both embryonic and tumor cells, but its activity appeared much more intense in the tumor cells. No ATPase was demonstrated in embryonic ectodermal cells of 6-day-old embryos and only in occasional cells of 7- and 8-day-old embryos. No 5'-nucleotidase activity could be demonstrated in 6- to 8-day-old cylinders. There was marked ATPase and 5'-nucleotidase activity in the membranes of embryonal carcinoma cells. These data point out some differences on the plasma membrane between the embryonal carcinoma cells and equivalent embryonic cells. The potential significance of these differences is discussed with regards to the transformation of embryonic cells in tumor cells. (Am J Pathol 87:297-310, 1977).
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PMID:Ultrastructural localization of membrane phosphatases in teratocarcinoma and early embryos. 19 83

Uvomorulin (E-cadherin), a cell adhesion molecule, and Na+,K(+)-adenosine triphosphatase (ATPase), a marker protein of the basal-lateral cell membrane domains of polarized epithelial cells, were investigated in a group of mouse skin tumors induced by a two-stage chemical carcinogenesis protocol and in cell lines derived from mouse skin papillomas and squamous cell carcinomas (SCC). Although these two markers were present in benign tumors and in nontumorigenic cell lines, the Na+,K(+)-ATPase showed an altered pattern of distribution that included the presence of enzyme not only in the basolateral domain but also on the apical domain of the cell membrane of basal and spinous cells in well-differentiated squamous cell carcinomas (SCC). In higher grade SCC, a loss of Na+,K(+)-ATPase immunoreactivity was simultaneously detected with a marginal or absent expression of uvomorulin. The more differentiated SCC and papillomas expressed less uvomorulin immunoreactivity than normal epidermal cells. Both markers were seen in tumor cell lines that produced well-differentiated SCC after subcutaneous inoculation into nude mice. Neither Na+,K(+)-ATPase nor uvomorulin could be detected in cell lines that produced high grade, poorly differentiated SCC. Northern blots confirmed the absence of uvomorulin mRNA in these highly malignant cell lines. These data indicate that progression from premalignant papilloma to low-grade SCC and subsequently to high-grade SCC is accompanied by loss of epithelial cell polarity as detected by changes in Na+,K(+)-ATPase and by decreased or absent expression of uvomorulin in tumors and cell lines characterized by an advanced malignant phenotype.
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PMID:Alterations in the expression of uvomorulin and Na+,K(+)-adenosine triphosphatase during mouse skin tumor progression. 131 85

Experiments were designed to determine the efficacy of different types of liver cell proliferative stimuli given during exposure to several liver tumor-promoting regimens, on the formation of foci of enzyme-altered hepatocytes. Male Wistar rats were initiated with diethylnitrosamine (150 mg/kg body wt). After a 2 week recovery period animals were subjected to promoting regimens, the resistant hepatocyte model, the phenobarbital model and the orotic acid model. While the rats were on these regimens they were given liver cell proliferative stimulus, either a compensatory type (two-thirds partial hepatectomy or a necrogenic dose of carbon tetrachloride) or a direct hyperplastic stimulus such as that induced by the primary mitogen, lead nitrate. Initiated cells so promoted by these regimens were monitored as foci of enzyme-altered hepatocytes positive for gamma-glutamyltransferase and placental glutathione S-transferase or deficient for adenosine triphosphatase. While carbon tetrachloride and partial hepatectomy-induced compensatory regeneration stimulated the promoting ability of the regimens used, direct hyperplasia could not stimulate the formation of foci and/or nodules from initiated hepatocytes. Evaluation of thymidine incorporation indicated that there was no significant difference in the extent of DNA synthesis in both the proliferative stimuli irrespective of the promoting procedure used.
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PMID:Mitogen-induced liver hyperplasia does not substitute for compensatory regeneration during promotion of chemical hepatocarcinogenesis. 134 15

Microtubules have been implicated as being necessary for the secretion of insulin from beta-cells, although the mechanism by which cytoplasmic microtubules contribute to the release of insulin is unknown. Kinesin is a microtubule-dependent adenosine triphosphatase (ATPase) that is thought to be responsible for the intracellular transport of vesicles and organelles. In this manuscript, the purification and preliminary characterization of a beta-cell form of kinesin is described. A 120-kilodalton antikinesin-reactive polypeptide was identified on blots when cultured insulinoma tumor cell lines were subjected to immunoblot analysis using monoclonal antibodies specific for the heavy chain of mammalian kinesin. The beta-cell form of kinesin was isolated from solid rat insulinoma tumors by cosedimentation of the kinesin with microtubules from tissue homogenates in the presence of adenylyl-imidodiphosphate. The beta-cell kinesin was further purified by gel filtration chromatography, and then the pure enzyme was characterized using in vitro assays. Although beta-cell kinesin showed little ATPase activity alone, the enzyme exhibited considerable ATP hydrolysis activity in the presence of taxol-stabilized microtubules. Moreover, in motility assays beta-cell kinesin was able to translocate microtubules across microscope coverslips in the presence of Mg(2+)-ATP. In summary, we report the identity of a novel islet beta-cell form of the microtubule-dependent ATPase kinesin and suggest a possible contribution of the microtubule cytoskeleton in insulin secretion.
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PMID:The identification, purification, and characterization of a pancreatic beta-cell form of the microtubule adenosine triphosphatase kinesin. 161 13

A 54-year-old man was admitted because of right supraclavicular lymphadenopathy of some weeks duration. Computed axial tomography revealed a large multinodular lesion in a supraclavicular lymph node. The patient then had a supraclavicular lymph node biopsy. Light microscopy showed a tumor whose structure was suggestive of an interdigitating cell sarcoma. Enzyme and immunohistochemical analysis showed that the tumor cells possessed membranous adenosine triphosphatase activity, intracytoplasmic S100 protein, surface CD1a and CD4 antigens, and HLA-DR antigen. Ultrastructural examination showed that the cells exhibited many interdigitating cytoplasmic extensions, but no Birbeck granules. DNA content analysis of the tumor cells proved that the cells were malignant. These data are consistent with derivation from a lymph node interdigitating cell.
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PMID:Lymph node interdigitating cell sarcoma. A case report. 172 55

Plasma membrane-associated adenosine triphosphatase (ATPase) samples partially purified from the tumor dissections of 15 gastric cancer patients were examined for sensitivity to the synthetic lignan, 2,3-dibenzylbutane-1,4-diol (hattalin), and ouabain in the presence of Mg2+, Na+, and K+. Hattalin was the strongest Na+, K(+)-ATPase inhibitor among the lignans previously examined. The enzyme from normal gastric tissue of the same patient was used as control. The specific activity of ATPase from cancer tissue (C-ATPase) was inhibited by more than 50% by 2.0 mM hattalin, whereas only 33.1% of the specific activity of ATPase from normal gastric mucosa (N-ATPase) was inhibited by 2.0 mM hattalin. There was statistical significance of lignan sensitivity between C- and N-ATPase (p less than 0.02). Ouabain also inhibited C-ATPase in preference to N-ATPase, though not significantly. Hattalin inhibited both C- and N-ATPase more strongly than did ouabain (p less than 0.05). Moreover, the lignan inhibited both C- and N-ATPase in the absence of Na+ and K+. From these data, it is evident that the sensitivity of plasma membrane-associated to lignan increased by gastric canceration. The target ATPase of hattalin is likely to be one other than sodium- and potassium-dependent, ouabain-sensitive ATPase.
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PMID:Differential sensitivity of human gastric cancer ATPase and normal gastric mucosa ATPase to the synthetic mammalian lignan analogue 2,3-dibenzylbutane-1,4-diol (hattalin). 183 Aug 24

The livers of rats given either the peroxisome proliferating hepatocarcinogen di(2-ethylhexyl)phthalate (DEHP) following initiation by 2-acetylaminofluorene (AAF) or the neoplasm promoter phenobarbital (PB) were studied for changes in 8 histochemical properties. Male F344 rats were fed 200 ppm AAF for 7 weeks to induce hepatocellular altered foci, and were then fed diets containing either no chemical, 12,000 ppm DEHP or 500 ppm PB for 24 weeks. In hepatocytes, DEHP increased alkaline phosphatase activity throughout the lobule, but reduced gamma-glutamyltransferase (GGT) activity in periportal hepatocytes. PB, in contrast, increased GGT activity in periportal hepatocytes. In foci that were induced by AAF, DEHP reduced the histochemical activity of GGT and did not increase the number, mean volume or volume % of foci detected by deficiencies in iron storage, glucose-6-phosphatase, adenosine triphosphatase or fibronectin. PB enhanced the expression of all 8 phenotypic abnormalities in foci such that either more profiles were detected or the area of foci was increased.
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PMID:Effects of the peroxisome proliferator di(2-ethylhexyl)phthalate on enzymes in rat liver and on carcinogen-induced liver altered foci in comparison to the promoter phenobarbital. 197 53

New growth of extraocular muscle has been demonstrated in degenerating peripheral nerve autografts implanted between two extraocular muscles. This suggests that extraocular muscle may be lengthened for therapeutic purposes if a suitable matrix can be found to support this new growth. Investigators of peripheral nerve regeneration have found that the basal lamina of freeze-killed skeletal muscle remains intact and supports axonal regeneration. This study was designed to investigate the feasibility of inducing regenerative growth of extraocular muscle in freeze-treated extraocular muscle autografts. In six beagles the inferior oblique muscle was removed from both orbits, frozen in liquid nitrogen, and allowed to thaw at room temperature. The freeze-thaw cycle was repeated. The freeze-treated grafts were then sewn in an end-to-end fashion between the cut end of the lateral rectus and the globe. At both 4 and 8 weeks postoperatively, three dogs were killed, and the grafts were removed from both orbits. These were prepared for light and electron microscopic examination. This revealed robust growth of mature-appearing, innervated muscle fibers in the proximal graft that could be differentiated by adenosine triphosphatase histochemistry. Rare, immature fibers were seen in the distal graft. These results demonstrate that freeze-treated extraocular muscle autografts support regenerative growth of extraocular muscle.
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PMID:Extraocular muscle regeneration in freeze-treated extraocular muscle autografts. 198 98

Within the acidic milieu of an abscess or tumor, macrophages must be able to maintain their cytoplasmic pH (pHi) close to the physiologic range to ensure optimal cell function. Our recent studies have demonstrated that a proton-extrusion mechanism with the characteristics of an H+ adenosine triphosphatase mediates pHi recovery in acid-loaded macrophages. These studies were designed to examine the role of these H+ pumps in maintaining cell function in an acidic extracellular environment. Peritoneal macrophages were tested for superoxide production in response to phorbol myristate acetate at either physiologic or acidic extracellular pH (pHo; 7.35 or 6.70, respectively). pHi was measured with the fluorescent dye 2',7'-biscarboxy-ethyl-5(6)-carboxy-fluorescein. Bafilomycin A1, a specific H+ adenosine triphosphatase inhibitor, was used to examine the contribution of the H+ pump to pHi regulation and cell function. At pHo 7.35, bafilomycin A1 had no effect on pHi or phorbol myristate acetate-stimulated superoxide production. However, at pHo 6.70, bafilomycin A1 reduced pHi to 6.61 +/- 0.01 versus 6.79 +/- 0.01 in control cells (p less than 0.001) and caused a concomitant reduction in superoxide production to 4.8 +/- 1.2 versus 13.0 +/- 1.2 nmol/10(6) cells/40 min in control cells (p less than 0.001). To determine whether the observed reduction in superoxide formation was the result of the pHi reduction, superoxide production was measured in cells whose pHi was pharmacologically clamped at various levels according to the K+/nigericin method. Lowering pHi from 6.80 to 6.60 caused a significant reduction in superoxide production from 13.1 +/- 1.8 to 7.5 +/- 0.9 nmol/10(6) cells/40 min (p less than 0.01). Thus H+ extrusion pumps are important to maintenance of macrophage pHi at low pHo, permitting continued superoxide production under these conditions. By keeping pHi close to the physiologic range, these pumps serve to optimize cell function in an acidic extracellular environment.
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PMID:Modulation of the macrophage respiratory burst by an acidic environment: the critical role of cytoplasmic pH regulation by proton extrusion pumps. 216 58

A human megakaryoblastic cell line, designated CHRF-288-11, has been established in vitro through the use of adherent stromal cells in long-term human bone marrow culture. Long-term bone marrow cultures were required for the initial adaptation of the megakaryoblastic cells to culture conditions; however, once adapted, the cells were weaned from the stromal layer until they proliferated in the complete absence of any feeder layers. The seed cells for the establishment of this line were derived from a solid tumor; the cloned cell line derived from this tumor exhibits markers characteristic of megakaryocytes and platelets. Specifically, the cells express platelet peroxidase, platelet factor 4, and platelet Ca+(+)-adenosine triphosphatase (ATPase), glycoprotein IIb-IIIa (CDw41), factor VIII antigen, and the MY7 (CD13) and MY9 (CD33) antigens. The cells do not express the erythroid markers glycophorin A and hemoglobin, the myeloid marker myeloperoxidase, nor markers specific for T and/or B cells. The established cell line produces both basic fibroblast growth factor and transforming growth factor-beta, properties demonstrated previously for the solid tumor. The clonal cell population exhibited a unique, singular karyotype, indicating cellular homogeneity. The cells display a doubling time of approximately 33 hours in either 25% horse or calf serum. Treatment of the cells with 1 X 10(-8) mol/L phorbol 12-myristate 13-acetate (PMA) leads to the induction of multi-nucleation and hyperploidy in the cells, with approximately 35% of the cells exhibiting two or more nuclei per cell, and greater than 80% of the cells enlarging in size. The establishment of this unique cell line under defined culture conditions will be beneficial for the future study of megakaryocytic properties expressed by this cell line.
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PMID:In vitro establishment and characterization of a human megakaryoblastic cell line. 231 Aug 25


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