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)

In addition to the previously described deoxyribonucleic acid (DNA) polymerase, DNA ligase, DNA exonuclease, and DNA endonuclease activities, purified virions of Schmidt-Ruppin strain of Rous sarcoma virus (SRV) have nucleotides and nucleotide kinase, phosphatase, hexokinase, and lactate dehydrogenase activities. The SRV virions have no glucose-6-phosphate dehydrogenase activity. All enzyme activities, but glucose-6-phosphate dehydrogenase and adenosine triphosphatase, were increased by disruption of the virions. The DNA polymerase, DNA ligase, and hexokinase activities had a higher specific activity in purified virion cores. It is suggested that during assembly virions of SRV may pick up cytoplasmic components which bind to virion proteins. The role of these components in viral replication is not known at present.
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PMID:Enzymes and nucleotides in virions of Rous sarcoma virus. 433 49

Cell lines resistant to ethidium bromide have been developed from cultured mammalian BHK21/C13 cells and these same cells transformed by Rous sarcoma virus (C13/B4). Cells resistant to 2 micrograms ethidium bromide per milliliter have been cloned. One clone of the control and one of the virus-transformed cell lines has been employed for characterization. The resistant cells, in the presence of 2 micrograms ethidium bromide/ml, grow at approximately the same rate as the untreated parental cells. The control cells possess a "normal" karyotype (44 chromosomes), while the corresponding ethidium bromide mutant has a reduced chromosome number of 41 and a number of translocations. The mitochondria displayed morphological alterations compared to the parental lines during the transition phase prior to the isolation of the ethidium bromide-resistant cells. The mitochondria of the ethidium bromide-resistant mutants appear somewhat enlarged with a normal morphology. The effect of ethidium bromide on selected respiratory enzymes in normal and virus-transformed ethidium bromide-resistant baby hamster kidney cells was determined. Ethidium bromide-resistant cells exhibited a depressed level of cytochrome aa3. This depression could not be reversed by growth in ethidium bromide-free media. Ethidium bromide-resistant cells possessed the same cytochrome b, c, and c1 levels per cell as their corresponding parental lines. Purified mitochondria isolated from virus-transformed ethidium bromide-resistant cells exhibited a depression in cytochrome oxidase-specific activity, while the ethidium bromide-resistant control cells did not. All cell lines studied showed a depression in NADH-ferricyanide and NADH-cytochrome c reductase-specific activities relative to their parental BHK21/C13 cells. No increase was observed in virus-transformed ethidium bromide-resistant cells. Ethidium bromide-resistant control cells exhibited a two-fold increase in oligomycin-insensitive adenosine triphosphatase activity relative to their parental cells. All of the cell lines studied possessed equivalent oligomycin-sensitive adenosine triphosphatase-specific activity except for the virus-transformed, dye-resistant mutant, whose activity was increased.
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PMID:Control and virus-transformed baby hamster kidney cells resistant to ethidium bromide. I. Characterization and the respiratory enzymes. 625 Oct 98

The increased rate of glucose uptake found in cells transformed by Rous sarcoma virus was shown to be enhanced relative to the changes in uptake induced in nontransformed cells by deprivation of glucose (deprivation derepression). Glucose-specific uptake sites were distinguished from glucose-galactose sites in nontransformed cells, and the capacities for glucose uptake and for galactose uptake were increased to about the same extent by the exclusion of glucose from the cell culture medium. Deprivation derepression occurred without a requirement for new RNA or protein synthesis, suggesting that preexisting inactivate uptake sites were activated. Deprivation derepression could be mimicked by the treatment of cells with adenosine triphosphatase activators, and adenosine triphosphate levels were reduced in glucose-deprived cells and in cells treated with adenosine triphosphatase activators. Cells transformed by the Bryan strain of Rous sarcoma virus were unresponsive to addition of high concentrations of glucose, to glucose starvation, or to treatment with adenosine triphosphatase activators, and the relative capacity for glucose uptake in these transformed cells was enhanced much more than the capacity of galactose uptake. It was concluded that cells infected by the Bryan strain of rous sarcoma virus in the process of transformation selectively synthesize more sites specific for glucose uptake. Lower levels of adenosine triphosphate found in transformed cells possibly contribute to a chronic derepression of uptake sites.
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PMID:Increased glucose uptake capacity of Rous-transformed cells and the relevance of deprivation derepression. 626 Mar 48