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:2.7.7.7 (DNA polymerase)
17,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection of mouse embryo cells with two strains of murine sarcoma virus and one strain of murine leukemia virus was followed rapidly by synthesis of DNA in the cytoplasm. Persistently infected cells have not shown such synthesis, and ultraviolet-irradiated virus did not induce DNA synthesis. This new DNA presumably represents an intermediate in the virus replication cycle specified by the virion DNA polymerase(s). Failure to observe cytoplasmic DNA synthesis in persistently infected cells suggests, in keeping with the results of inhibitor experiments, that the new "viral" DNA becomes associated with cellular DNA in some form of stable interaction.
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PMID:Cytoplasmic DNA synthesis induced by RNA tumor viruses. 433 62

Infection of duck embryo fibroblasts by Marek's disease herpesvirus (MDHV), strain GA, led to the induction of a novel DNA polymerase. This novel DNA polymerase, designated MDHV-induced DNA polymerase, could be distinguished from the DNA polymerase activities of uninfected duck embryo fibroblasts by its chromatographic behavior on phosphocellulose, by its sedimentation coefficient, and by its catalytic properties. The characteristics of MDHV-induced DNA polymerase which had been purified by phosphocellulose chromatography were investigated. The sedimentation coefficient of the enzyme, as determined by sucrose density gradient centrifugation in the presence of 0.25 M KCl, was 5.9S. From this sedimentation coefficient, the molecular weight of MDHV-induced DNA polymerase was estimated to be 100,000. MDHV-induced DNA polymerase could not effectively use either poly(dA).oligo(dT)(12-18) or poly(dC).oligo(dG)(12-18) as a template-primer. The DNA polymerases from uninfected duck embryo fibroblasts could use these synthetic template-primers. MDHV-induced DNA polymerase also could not use poly(rA).oligo(dT)(12-18) or poly(rC).oligo(dG)(12-18) as template-primers or oligo(dT)(12-18) as a primer, indicating that it was not a polymerase of the type R-DNA polymerase, reverse transcriptase, or a terminal nucleotidyl transferase. In vitro synthesis of DNA by MDHV-induced DNA polymerase was markedly inhibited by the addition of (NH(4))(2)SO(4) to the reaction mixture.
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PMID:Marek's disease herpesvirus-induced DNA polymerase. 447 69

SPO2 and phi105 are temperate Bacillus subtilis bacteriophages which have been suggested to belong to a cluster of related bacteriophages. In the present work, we show that SPO2 does not complement any of the 11 essential genes known in phi105 and that the phages do not recombine. Deoxyribonucleic acid (DNA)-DNA hybridization shows less than 10% homology between SPO2 and phi105 DNA. DNA synthesis in phi105 shows a greater dependence on host functions than does SPO2 DNA synthesis. Growth of phi105 but not of SPO2 is inhibited by the uracil analogue 6-(p-hydroxyphenylazo)-uracil. Infection of a DNA polymerase-deficient strain of B. subtilis with SPO2 leads to an increase in DNA polymerase activity in crude extracts, whereas no such increase is found after infection of this strain with phi105. It is concluded that SPO2 and phi105 are unrelated bacteriophages.
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PMID:Unrelatedness of temperate Bacillus subtilis bacteriophages SP02 and phi105. 462 14

Increased deoxyribonucleic acid (DNA) polymerase activity is found in soluble extracts from a polymerase I-negative mutant of Bacillus subtilis after infection with temperate phage SPO2, or after induction of SPO2 prophage in lysogenic derivatives of this mutant. No increased enzyme activity is found after SPO2 infection in the presence of chloramphenicol. Infection of the polymerase-negative mutant with the DNA-negative sus mutant SPO2 L244 gives no increased enzyme activity, whereas infection with DNA-negative sus mutant SPO2 J385 gives enzyme activities comparable to those found in wild-type infected cells. These findings suggest that SPO2 determines a DNA polymerase activity essential for synthesis of phage DNA.
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PMID:Deoxyribonucleic acid polymerase activity in a deoxyribonucleic acid polymerase I-deficient mutant of Bacillus subtilis infected with temperature bacteriophage SPO2. 462 7

Previous studies on the biological effects of the 2',3'-dideoxynucleosides (ddNs) have shown that while ddAdo is lethal to E. coli, ddThd has minimal effects on the growth of mammalian cell lines and that it inhibits retrovirus infection of some cell lines but not others. Previous studies have also shown that the 5'-triphosphate of ddThd, ddTTP, selectively inhibits cellular DNA polymerases beta and gamma and retroviral reverse transcriptases. Cellular DNA polymerase alpha is relatively resistant to ddTTP. We have extended these findings to show that the 5'-triphosphates of the other 3 ddNs (ddATP, ddCTP, and ddGTP) affect cellular DNA polymerases alpha, beta, and gamma in the same fashion as does ddTTP. We also show that all four ddNs in concentrations up to 100 microM have negligible effects on the growth of NIH Swiss 3T3 cells. These negligible effects may be due to inefficient intracellular phosphorylation of each nucleoside to the triphosphate. We have determined that, in several different cell lines, ddThd is phosphorylated only at a very slow rate to ddTTP, and in the one cell line tested (monkey CV-1 cells), ddAdo and ddGuo are also poorly phosphorylated. Both ddAdo and ddGuo, and probably ddThd, are converted by CV-1 cells to additional unknown compounds which may have biological activity. The four ddNs display effects of different magnitudes on certain virus infections. Although 30 microM ddThd inhibits herpes simplex I infection of CV-1 cells by 50%, 30 microM ddAdo has no effect. Infection of NIH Swiss 3T3 cells by 334C murine leukemia virus is inhibited 70-80% by ddAdo, ddCyd, and ddThd at 50 microM, but inhibition by 50 microM ddGuo is 100%.
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PMID:Effects of 2',3'-dideoxynucleosides on mammalian cells and viruses. 609 93

Infection with herpes simplex viruses (HSV) lead to a significant increase of the simian virus 40 (SV40) DNA content in the SV40-transformed hamster cell lines CO631 and Elona. Analysis of this gene-amplifying activity revealed (i) that it cosedimented with infectious herpesvirions in sucrose density gradients, (ii) that it was abolished by anti-HSV antibodies or (iii) by antiviral drugs acting on the HSV-induced DNA polymerase; and analysis of temperature-sensitive mutants showed that this DNA polymerase was an essential component of HSV-induced, gene-amplifying activity in SV40-transformed hamster cells.
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PMID:Identification of a gene function of herpes simplex virus type 1 essential for amplification of simian virus 40 DNA sequences in transformed hamster cells. 610 May 73

Two forms of ribonuclease H (RNase H) have been identified both in uninfected and Herpes Simplex virus (HSV-)infected BHK cells. Identical RNase H species were detected in control- as well as in infected cells. RNase H I and II have not been found to be associated both with host cell DNA polymerase alpha and beta and HSV-induced DNA polymerase. Infection of BHK cells with HSV type 1 does not lead to a pronounced alteration of RNase H II activity but to an increase (3-fold) of the extractable RNase H I activity. RNase H I activity increases to a maximum between 8-10 hours p.i.; the bulk of HSV-DNA synthesis occurs between 6-8 hours p.i. From these experiments we draw the preliminary conclusion that RNase H I is involved in the degradation of the RNA primer which is covalently linked to newly synthesized HSV-DNA strands.
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PMID:Ribonuclease H levels in herpes simplex virus-infected cells. 625 May 16

The association of human cytomegalovirus with mink and rabbit lung cells was studied. Strain AD-169 was used which was free of Mycoplasma and other contaminating agents. It was found to be incapable of productively infecting mink lung cells. Infection appeared to be initiated but aborted at an early stage. This was indicated by indirect immunofluorescence, assays of culture supernatants and cell lysates for infectious virus, electron microscopy of ultra-thin sections of infected cells, labelling of virus and viral DNA with 3H-thymidine and assay of virally-induced DNA polymerase at various times after infection. On the other hand, using these methods. AD-169 was found to infect rabbit lung cells, the virus being produced in low amounts over a period of up to one month after infection. At this time, focal areas of infection were still apparent and 15 per cent of the cells expressed nuclear viral antigens as shown by immunofluorescence. The viral genome was assumed to have become latent in some rabbit cells with a few being capable of producing infectious virus.
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PMID:Association of human cytomegalovirus (HCMV) with mink and rabbit lung cells. 626 19

The stimulation of host cell DNA synthesis was studied in permissive human embryonic lung (HEL) cells and in nonpermissive rabbit kidney (RK) cells infected with human cytomegalovirus (HCMV). Host cell DNA synthesis was induced by HCMV infection in resting cells of both types. In permissive cultures the stimulation of cellular DNA synthesis was detectable mainly in those cells which had not become productively infected and in which virus antigens were not detectable. In abortively infected RK cells, on the other hand, stimulation of host cell DNA synthesis and the expression of virus antigens were detected in the same cells. Infection of actively growing permissive HEL cells resulted in a shutdown of cellular DNA synthesis beginning approximately 10 hr postinfection. Shutdown of cellular DNA synthesis also occurred when the infected cells were treated with phosphonoacetic acid and was thus classified as an "early" virus function. In actively growing, abortively infected RK cells, on the other hand, host cell DNA synthesis was not affected, indicating that the early virus function(s) responsible for inhibition of cellular DNA synthesis was not expressed in these cells. Virus-encoded DNA polymerase activity, another early virus gene function, was also not detected in these abortively infected cultures. In RK cells the cellular DNA synthesized as a result of infection was capable of undergoing at least one further round of replication, indicating that the HCMV gene expression which occurred in abortively infected RK cells was not lethal for these cells.
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PMID:Correlation between stimulation of host cell DNA synthesis by human cytomegalovirus and lack of expression of a subset of early virus genes. 631 75

The HBeAg/anti-HBe system was studied as a marker of infectivity and chronic progressive liver disease in 460 hemodialysis patients. The importance of HBeAg as an index of infectivity was confirmed in that it was present simultaneously with specific DNA polymerase (31 patients) and by the presence of widely diffuse core particles in the hepatocyte nuclei (revealed by biopsy in six patients). In contrast, HBeAg showed no useful correlation with progressive liver disease, the absence of which was confirmed in all cases by biochemical and histological studies.
Infection
PMID:The significance of the HBeAg/anti-HBe system in hemodialysis patients. A multicenter study. 636


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