Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.49 (reverse transcriptase)
 31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Revertants of nonproducer human osteosarcoma (NP/KHOS) cells induced by Kirsten murine sarcoma virus were isolated after incubating at high temperature (40.5 degrees C) overnight and subcloning at 36 degrees C. The morphologic variants, from which murine sarcoma virus could no longer be rescued, had growth properties similar to those of the nontransformed, parent human osteosarcoma cells and did not release RNA-dependent DNA polymerase activity. These revertants were nontumorigenic in nude mice. The revertants supported leukemia virus growth and showed an enhanced sensitivity to murine sarcoma virus superinfection. Thus, the revertants were from human cells transformed by an oncogenic RNA virus.
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PMID:Revertants of human cells transformed by murine sarcoma virus. 6 97

Increasing evidence has accumulated that the direct assay of reverse transcriptase in human blood cells is of value in the diagnosis of leukaemia. The isolation and characterization of this enzyme has shown that it possesses remarkable similarities to the DNA-polymerase of the RNA-tumour virus of simian sarcoma. Hence, leukaemic cells in humans are thought to possess a virus-related gene, namely, reverse transcriptase. Various clinical reports have established the presence of this enzyme in blood cells, not only in the case of morphologically-proven malignant change, but also in cases classified as non-leukaemic from the morphological picture, such as acute leukaemia in remission and in the pre-leukaemic state. In confirmation and augmentation of earlier views we now report on the presence of reverse transcriptase in a patient with pancytopenia, who subsequently developed acute leukaemia i.e. isolation of the enzyme occurred in the pre-leukaemic state.
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PMID:[New polymerase gene in pancytopenia (author's transl)]. 6 82

Murine Rauscher leukemia virus (MuRLV) from BALB/c plasma consisting of a mixture of an ecotropic and a xenotropic virus could be separated out by a selection process when propagated in human and simian cell cultures. This hypothesis is supported by obtaining consistently lower infectivity titers of human cell propagated RLV in human and simian cells as compared to MuRLV propagated in mouse cell cultures. Furthermore, RLV passaged in a simian cell culture failed to replicate in mouse cells, had a wide host range, was able to rescue Moloney sarcoma genome, possessed murine type C group-specific antigen, and was neutralized by anti-HRLV. Its reverse transcriptase was strongly inhibited by antiserum to MuRLV enzyme; however, antiserum to woolly monkey enzyme also inhibited (30%) its reverse transcriptase, suggesting some difference in antigenic properties. Inoculation of this virus in rhesus monkeys was inconclusive.
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PMID:Xenotropic properties of an isolate from murine Rauscher leukemia virus in primates. 6 54

Ethidium bromide (2,3-diamino-5-ethyl-6-phenylphenanthridinium bromide) significantly inhibited the RNA-dependent DNA polymerase of types A and C particles isolated from transplanted adenovirus 12-induced tumors of CBA mice. It was also cytotoxic for an established in vitro line of adenovirus 12-induced tumor cells of CBA mice and caused cell death, inhibition of [3H]thymidine uptake, and a significant reduction of cells in metaphase. Ethidium bromide significantly inhibited the in vivo growth of transplanted adenovirus 12-induced tumor cells of CBA mice, simian virus 40-induced tumor cells of hamsters, and murine leukemia virus-induced lymphoma cells of BALB/c mice. The compound may have exerted the antitumor activity by selectively affecting oncornavirus in the tumor cells.
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PMID:Effect of ethidium bromide on transplanted virus-induced tumor cells. 6 62

The degree of inhibition of mammalian DNA-dependent RNA polymerases I and II and Moloney leukemia virus RNA-dependent DNA polymerase by pyran copolymer was dependent on the concentration of the divalent cation cofactor in the reaction mixture. Inhibition was completely blocked by an excess of divalent cations. It was concluded that pyran inhibited these enzymes by complexing with the essential divalent cation cofactor.
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PMID:Role of divalent ion complex formation in pyran--inhibition of nucleic acid biosynthesis. 6 66

Somatic cell hybrids were constructed between BALB/c-RAG mouse cells and feline lymphoma cells by the hypoxanthine-aminopterin-thymidine selection scheme. RAG cells spontaneously produce an endogenous B-tropic type C virus. Cat-mouse hybrids preferentially segregate feline chromosomes and retain murine chromosomes-demonstrable by karyotypic and isozyme analyses. Despite the presence of the complete mouse genome, including the viral genome, virus production was diminished to 1-5% of the levels observed in RAG parents based upon particle-associated RNA-dependent DNA polymerase (reverse transcriptase) activity in the culture fluid. Thirty-seven hybrids made on four different occasions had suppressed virus levels, and no hybrids expressed parental virus levels. Reverse selection experiments on 6-thioguanine demonstrated that a restriction gene, tentatively named Bvr-1, was linked to the feline structural genes for hypoxanthine phosphoribosyltransferase (IMP:pyrophosphate phosphoribosyltransferase; EC 2.4.4.8) and glucose-6-phosphate dehydrogenase (D-glucose-6-phosphate: NADP+ 1-oxidoreductase; EC 1.1.1.49) in cats, probably on the X-chromosome. The genetic mode of action of Bvr-1 is trans dominant in restriction of murine leukemia virus. The restriction locus results in a block late in virus maturation but prior to release, since expression of antigens for viral structural proteins and matrue budding particles is apparent on surfaces of restriced hybrid cells but not in high-speed pellets from culture fluid of restricted cells.
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PMID:Bvr-1, a restriction locus of a type C RNA virus in the feline cellular genome: identification, location, and phenotypic characterization in cat X mouse somatic cell hybrids. 6 49

Short term cultures of bovine leukemic lymphocytes release virus particles with biochemical properties of RNA oncogenic viruses. These particles, tentatively called Bovine Leukemia Virus (BLV) have a high molecular weight-reverse transcriptase complex and a density averaging 1.155 g/ml in sucrose solutions. Molecular hybridizations between BLV-3H cDNA and several viral RNAs show that BLV is not related to Mason-Pfizer Monkey Virus (MPMV) Simian Sarcoma Associated Virus (SSV-1) Feline Leukemia Virus (FeLV) or Avian Myeloblastosis Virus (AMV). Rauscher Leukemia Virus (RLV) exhibits a slight but reproducible relatednesse to BLV. The high preference of BLV reverse transcriptase for Mg++ as the divalent cation suggests that BLV might be an atypical mammalian leukemogenic type C virus. Hybridization studies using BLV 3H cDNA as a probe suggest that the DNA of bovine leukemic cells contains viral sequences that cannot be detected in normal bovine DNA.
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PMID:Bovine leukemia virus: an exogenous RNA oncogenic virus? 6 82

Rauscher leukemia virus RNA-directed DNA polymerase has been purified to near homogeneity (greater than 90% pure) using affinity chromatography on polycytidylate-agarose with over 85% recovery of input enzymatic activity. The purified enzyme has a molecular weight of approximately 70,000 and appears to consist of a single polypeptide chain. The enzyme is free of DNase, but has RNase H activity. Analysis of the requirements for optimal rates of DNA synthesis by this enzyme using synthetic and natural template-primers has revealed template-specific variations in such requirements. During these studies it was observed that DNA synthesis catalyzed by Rauscher leukemia virus DNA polymerase is inhibited by the addition of inorganic phosphate. An analysis of the mechanism of phosphate inhibition was carried out using the synthetic template-primer poly(A)-(dT)10. It appears that by some mechanism, possibly involving the substrate binding site of the enzyme, phosphate ions inhibit DNA synthesis with a more acute effect on the rate of chain growth than on that of initiation. The extension of these studies to DNA synthesis catalyzed by a variety of mammalian type C viral reverse transcriptases revealed that low levels ( less than or equal to 2 mM) of inorganic phosphate strongly inhibited DNA synthesis. The susceptibility to phosphate inhibition appears unique to mammalian type C viral enzymes since the type B viral enzyme, Escherichia coli DNA polymerase I, avian myeloblastosis virus and Mason Pfizer monkey tumor virus reverse transcriptase and cellular DNA polymerases alpha and gamma are not inhibited by inorganic phosphate. This phenomenon of phosphate inhibition of various DNA polymerases, therefore, provides a new basis for the differentiation of the sources and nature of these enzymes.
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PMID:Purification and properties of Rauscher leukemia virus DNA polymerase and selective inhibition of mammalian viral reverse transcriptase by inorganic phosphate. 6 68

The mode of action of interferon in de novo Moloney murine leukemia virus (Mo-MuLV) infection of mouse bone marrow/thymus (TB) cells was studied. Our results indicate that in interferon-treated cells, there is approximately a 2000 fold decrease in the production of infectious MuLV, but only a 10-20 fold decrease in the level of viral specific extracellular reverse transcriptase activity, and only about a 2 fold difference in the number of virus particles observed on the cell membrane as determined by scanning electron microscopic (SEM) studies. Transmission electron microscopic (TEM) studies showed that the proportion of early budding virions, which have shallow crescent-shaped ribonucleoprotein cores (Figure 3A), to virions in later stages of assembly (Figures 3B-3D) is relatively higher in interferon-treated cells than in the untreated controls. From a temperature shift-down experiment on a temperature-sensitive mutant of MuLV, ts 3, which produces viral particles that fail to dissociate from the cell surface at the nonpermissive temperature, we demonstrated that ts 3 virions partially assembled on the cell membrane prior to the addition of interferon are able to complete assembly and to dissociate from the cell membrane on temperature shift-down in the presence of interferon action. Our data suggest that interferon neither inhibits the late stages of virion assembly at which ts 3 virions are arrested at the nonpermissive temperature nor prevents release of the virions. Our findings also indicate that in interferon-treated cells, most of the extracellular virions are noninfectious.
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PMID:The effect of interferon on de novo infection of Moloney murine leukemia virus. 6 31

The Friend erythroleukemia cell line T3-C12, which produces Friend murine leukemia virus (F-MuLV) and can be induced to synthesize hemoglobin by dimethyl sulfoxide (DMSO), was monitored for viral RNA-dependent DNA polymerase reverse transcriptase (RT) activity. The amount of viral 60-70S RNA released from DMSO-treated cells was unaffected or increased compared to that from control cells, while RT activity from treated cells was decreased. Accordingly, the specific activity in F-MuLV from DMSO-treated cells expressed as RT/70S RNA was decreased to 8% of the control activity. The 5-bromo-2'-deoxyuridine added to cultures containing DMSO reversed the differentiation process, and the F-MuLV thus treated did not exhibit the reduced RT activity normally observed in DMSO-treated virus. Cell-free F-MuLV incubated with and without DMSO showed the same RT activity, indicating that DMSO itself did not inhibit RT activity. However, when F-MuLV-containing pellets from control and DMSO-treated culture fluids were mixed, there was marked inhibition of the control RT activity, suggesting that RNase hybrid activity was stimulated or that an inhibitor was produced. Assays of F-MuLV-RNase hybrid released from control and DMSO-treated cells showed no difference in activity, indicating that a specific inhibitor of RT was produced or activated. Additions of certain nucleotide triphosphates to RT incubation mixtures did not result in any stimulation of RT activity in DMSO-treated F-MuLV, suggesting that phosphatase was not responsible for the observed inhibition. The results suggested that DMSO treatment of T3-C12 cells caused a reduction in viral RT activity by stimulating the production of an inhibitor, the nature of which is unknown.
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PMID:Viral reverse transcriptase suppression associated with erythroid differentiation of Friend leukemia cells. 6 77


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