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)

A cell surface-located nucleoside triphosphatase activity can be assayed in liver epithelial cultures in situ with the incubation of intact cells in a medium containing [gamma-32P]adenosine triphosphate and correlated with the tumorigenicity of these cells in neonatal Wistar rats. The ectoenzyme activity of normal diploid cell lines is minimal, whereas a considerably high activity has been found in all tumorigenic cell lines tested. The optimum condition for the adenosinetriphosphatase activity is physiological with regard to osmolarity, ionic composition, pH, and substrate concentration in the medium. The enzyme is significantly stimulated by Ca2+, and its activation is controlled by Mg2+. Histochemical examinations indicate that glutaraldehyde-fixed cells of tumorigenic lines have Ca2+-stimulated adenosinetriphosphatase activity on the external surface. The isotopic assay of adenosine triphosphate hydrolysis by intact cells may provide a rapid method for screening oncogenesis in vitro of liver epithelial cells.
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PMID:Surface membrane nucleoside triphosphatase activity and tumorigenicity of cultured liver epithelial cells. 13 72

Resting and active-state respiratory velocities, respiratory control, high amplitude volume changes, and latent ATPase activities were examined in hepatic mitochondria from rats fed 3'-methyl-4-dimethylaminoazobenzene (3'MeDAB) for production of liver tumors and from rats in three phases of liver regeneration subsequent to subtotal hepatectomies. Tetrabutylammonium bromide, a lipophilic probe capable of selectively inhibiting phosphorylating oxidation or uncoupling oxidation from phosphorylation, was used to detect subtle alterations in lipophilicity characteristics of the organelles and it was concluded that mitochondria from pre-hyperplastic, hyperplastic, and neoplastic tissues had a higher than normal degree of membrane lipophilicity at specific functional sites. Control of respiration by ADP was markedly augmented in all experimental groups; this behavior, plus depressed sensitivity to swelling agents and energized contraction, were similar in mitochondria from hepatomas and from 3-day regenerating livers. These mitochondrial functions were even more pronounced, however, in cells in pre-hyperplastic states (6 and 16 h subsequent to partial hepatectomy). Many forms of liver damage result in mitochondrial alterations which elevate the capacity for oxidative phosphorylation. Such changes associated with induction of azo dye oncogenesis are mimicked by the degree of hyperplasia in the tissue following the first mitotic wave of regeneration; implications relevant to hepatocarcinogenesis are discussed.
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PMID:Mitochondrial functional changes during hepatic hyperplasia and azo dye carcinogenesis. 17 55

Using electrophysiological techniques we have examined the apical membrane ionic permeabilities of primary cell cultures of the mouse mammary gland in the midpregnant, preneoplastic, and neoplastic states. Membrane Na+ permeability changed with tumorigenesis, whereas K+ and Cl- permeabilities were unaltered. With tracer flux techniques the unidirectional efflux rate constant of 22Na was found to be greater in tumor cells than it is in normal cells. This increase in 22Na efflux was eliminated by the addition of ouabain. The results are interpreted as an increase in Na+ permeability and in Na+-K+-ATPase activity with the neoplastic transformation. The presence or absence of the virus in midpregnant cells does not seem to affect Na+ permeability.
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PMID:Alteration of sodium transport in mouse mammary epithelium associated with neoplastic transformation. 20 64

Pituitary tumorigenesis occurs in a transgenic line of mice, alpha-T7, which carries a hybrid transgene composed of the 5' flanking region of the human glycoprotein hormone alpha-subunit gene (1.8 kb) linked to the coding region of the SV40 T-antigen gene (alpha-Tag). Tumor foci were identified within the anterior pituitary of both male and female transgenic mice. In addition to a parenchyma with hypertrophied endocrine cells, mostly of the gonadotrope lineage, we here report the unexpected presence of neural tissue within the anterior pituitary, either as foci as large as 1.0 mm in diameter or greater, or in delicate bundles ramifying amongst the granulated parenchymal cells. Areas richest in neural tissue frequently were associated with tumor tissue composed of giant cells of three varieties, all with electron-lucent cytoplasm and similar organellar distribution including small secretory granules (80-160 nm diameter). In type I cells, the secretory granules were aligned at the plasma membrane; in type II cells, the secretory granules were distributed throughout the cytoplasm; type III cells formed colloid-filled follicles and their secretory granules rarely exceeded 100 nm diameter. These giant cells frequently had bizarre pleomorphic nuclei intensely immunopositive for T-antigen and cytoplasm which was lightly immunopositive for alpha-subunit, and immunopositive either for the LH-beta or TSH-beta subunits. Neural tissue contacted the normal granulated parenchymal cells directly, i.e., without a basal lamina or any connective tissue intervening, but only rarely formed synaptoid junctions with these granulated cells. Synaptoid junctions containing round, smooth vesicles, as well as dense core vesicles, were numerous between the neural processes themselves and between the neural tissue and the giant cells of the tumor tissue. These data suggest that in alpha-T7 transgenic mice the giant cells represent highly transformed gonadotropes or thyrotropes, and that a neurotrophic factor may be expressed by these transformed pituitary parenchymal cells.
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PMID:Neural tissue within anterior pituitary tumors generated by oncogene expression in transgenic mice. 133 36

We have found a substantial decrease in the level of Na,K-ATPase beta 2-subunit mRNA in xenografts of human renal, lung hepatocellular carcinomas in nude mice as compared with corresponding normal tissues, as well as in the neuroblastoma cell line as compared with the neuron primary cell culture. The level of beta 1 mRNA is decreased in kidney and lung tumor cells, but is unchanged in hepatocellular carcinoma. In the neuroblastoma cell line the level of beta 1 subunit mRNA was found to be higher then in neuron primary cell culture. The level of alpha 1 mRNA in investigated tumors was the same as in normal tissues. These results may give evidence of the involvement of beta 2-subunit in the process of tumorigenesis as was shown for some other adhesion molecules.
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PMID:Tissue-specific expression of Na,K-ATPase beta-subunit. Does beta 2 expression correlate with tumorigenesis? 165 77

We present a murine model of trilateral retinoblastoma. Ocular retinoblastoma and central nervous system tumors are observed in a line of mice formed by the transgenic expression of SV40 T-antigen. An oncogenic protein known to bind to the retinoblastoma gene product (p105-Rb) is specifically expressed within retinal cells in this model. All animals that carry this genetic alteration develop multifocal retinal tumors. Midbrain tumors are observed in 15% of ocular tumor-bearing animals, and these arise ventral to the cerebral aqueduct at the level of the pineal gland. Both ocular and central nervous system neoplasms are heritable in heterozygous offspring through 10 sequential generations of breeding. Retinal tumors display the gross appearance, invasive properties, light and electron microscopic features, and immunohistochemical staining characteristics of human retinoblastoma. The light and electron microscopic characteristics as well as immunocytochemical features of undifferentiated midline central nervous system neoplasms further correlate with human trilateral retinoblastoma. We postulate an alternative mechanism of retinoblastoma tumorigenesis that involves functional inactivation of retinoblastoma protein locally in the face of an intact retinoblastoma gene locus.
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PMID:A transgenic mouse model for trilateral retinoblastoma. 169 69

Injection into nude mice of a well-differentiated SV40 T-antigen-transformed murine endothelial cell (EC) line results in widespread invasive tumors confined to connective tissues. The tumors, which do not metastasize, consist of both host-derived cells and transformed EC, displaying histologic features typical of Kaposi's sarcoma (KS). Although the EC is believed to be the cell of origin in KS, this has not been proven and is the subject of debate. The unusual tumorigenicity of this transformed cell suggests that EC-specific gene products induced by SV40 T antigen may contribute to tumorigenesis by autocrine growth stimulation and recruitment of host cells. KS-like tumors may be the result of EC alteration by any virus that induces relevant EC-derived cytokines.
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PMID:Endothelial cells transformed by SV40 T antigen cause Kaposi's sarcomalike tumors in nude mice. 192 99

By genetically targeting tumorigenesis to specific hypothalamic neurons in transgenic mice using the promoter region of the gonadotropin-releasing hormone (GnRH) gene to express the SV40 T-antigen oncogene, we have produced neuronal tumors and developed clonal, differentiated, neurosecretory cell lines. These cells extend neurites, express the endogenous mouse GnRH mRNA, release GnRH in response to depolarization, have regulatable fast Na+ channels found in neurons, and express neuronal, but not glial, cell markers. These immortalized cells will provide an invaluable model system for study of hypothalamic neurosecretory neurons that regulate reproduction. Significantly, their derivation demonstrates the feasibility of immortalizing differentiated neurons by targeting tumorigenesis in transgenic mice to specific neurons of the CNS.
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PMID:Immortalization of hypothalamic GnRH neurons by genetically targeted tumorigenesis. 219 69

Transgenic mice that contain the simian virus 40 (SV40) enhancer-promoter and large tumor (T) antigen gene develop papillomas of the choroid plexus. The tumors remain well differentiated on histological examination and express normal levels of tissue-specific mRNAs for transthyretin (TTR) and the 5-HT1C serotonin receptor, two differentiated cell markers. Both Northern (RNA) blot analysis and in situ cytohybridization have been used to monitor the steady-state levels of the mRNAs from the viral oncogene (T antigen) and from several cellular oncogenes. In situ hybridization demonstrated, in serial sections, increased levels of both T antigen mRNA and p53 mRNA localized in the tumor tissue but not in the normal brain tissue. The ratios of the steady-state levels of mRNA for p53/TTR and p53/L32, a ribosomal protein gene, were 2- to 20-fold higher in the tumor tissue than in the normal choroid plexus tissue. Several other oncogenes did not show elevated levels of mRNA in these tumors. p53 protein levels were not detectable in normal brain tissue, but p53 levels were very high in tumor tissue in which all of the p53 was found in a complex with the SV40 large T antigen. These data continue to show a close relationship between SV40 T-antigen-mediated tumorigenesis and the role of p53 in these tumors.
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PMID:Cellular gene expression in papillomas of the choroid plexus from transgenic mice that express the simian virus 40 large T antigen. 264 78

Tissue-specific tumorigenesis can be induced in transgenic mice by the directed expression of simian virus 40 (SV40) large tumor (T) antigen. In an attempt to determine the susceptibility of haploid, round spermatids to neoplastic transformation by this oncogene, transgenic mice were generated that harbored a chimeric gene composed of the SV40 T-antigen genes fused to the 5' and 3' flanking sequences of the mouse protamine 1 gene. The transgene was expressed in round spermatids and, surprisingly, in the heart and temporal bone as well. Expression in the heart resulted in rhabdomyosarcomas that always appeared in the right atrium. Bilateral osteosarcomas developed within the petrous portion of the temporal bone. No testicular pathology was observed. T-antigen immunostaining was readily detected in tumor tissue but not in the testis. In addition, SV40 transcripts were processed differently in testis and tumor tissue. Transgenic mouse lines were established that routinely develop these tumors, and they should provide a valuable resource for studies involving cardiac and bone physiology and neoplasia. The atrial tumor cells can be maintained in vitro and some continue to display a cardiac muscle phenotype.
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PMID:Heart and bone tumors in transgenic mice. 283 48


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