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)

Mild detergent treatment (0.1% Sarkosyl-0.1% beta-mercaptoethanol) of Dane particle-rich fraction from human serum resulted in the release of core particles together with HBe antigen activity when examined by the reversed passive haemagglutination method. Furthermore, when the core particles isolated by the above procedure were exposed to stronger detergent (1% Sarkosyl-0.1% beta-mercaptoethanol), additional HBe antigen activity was released only from intact core particles with DNA polymerase activity and not from empty core particles.
J Gen Virol 1979 May
PMID:Demonstration of hepatitis B e antigen (HBeAg) in association with intact Dane particles. 11 99

lambdapolA phages carrying the polA gene in either orientation were isolated and characterised by genetic tests and by assay of the polA gene product after infection of E. coli or induction of lysogens. Lytic infection gave consistently better amplification of DNA polymerase I than that obtained by induction of a lysogen. Optimal amplification of DNA polymerase I was not achieved from the PL promoter of cro-phages, but some advantages accrued when the polA gene was oriented for transcription from the PL promoter of a cro+ phage. lambdapolA phages in which the polA allele was from E. coli strain C600 provided better amplification than phages with the polA allele from E. coli ED8659. Induction of a lambdapolA1 cI857 Qam Sam prophage gave levels of DNA polymerase I approaching 100 times that found in the non-lysogenic Pol+ host. Genetics studies with the lambdapolA phages confirmed the previously postulated orientation of the polA gene within the E. coli genome.
Mol Gen Genet 1979 Aug
PMID:Characterization of lambdapolA transducing phages; effective expression of the E. coli polA gene. 15 99

The DNA polymerase activity in BHK 21/C13 cells infected with pseudorabies virus is inhibited by incubation with antiserum to pseudorabies but not by incubation with pre-immune serum or by antiserum to herpes simplex virus type 1 (HSV-1) or herpes simplex virus type 2 (HSV-2). It also differs from the cell enzyme and the enzymes in HSV-1 or HSV-2 infected cells in its requirement for KCl in the in vitro assay. It seems likely, therefore, that pseudorabies virus specifies its own DNA polymerase.
J Gen Virol 1976 Jan
PMID:DNA polymerase in pseudorabies virus infected cells. 17 98

Three mutants of herpes simplex virus (HSV) have been isolated which form plaques in the presence of 100 mug/ml phosphonoacetic acid (PPA). All three mutants (3 from HSV-1 strain 17 syn+, 14 from HSV-1 strain 17 syn, and 19 from HSV-2) induce viral DNA synthesis and viral DNA polymerase activity, and these are much less sensitive to PPA than the wild-type virus. The results support the hypothesis that PPA interacts directly with the viral DNA polymerase protein, at least part of which is virus coded.
J Gen Virol 1976 Apr
PMID:Mutants of herpes simplex virus types 1 and 2 that are resistant to phosphonoacetic acid induce altered DNA polymerase activities in infected cells. 17 27

Eleven temperature-sensitive mutants of herpes simplex virus type 2 strain HG52 were examined for ability to induce DNA polymerase activity in BHK 21/C13 cells. All mutants induced DNA polymerase at a permissive temperature, (31 degrees C) and all DNA-positive mutants at a non-permissive temperature (38 degrees C). Three DNA-negative mutants induced no DNA polymerase (ts 6, ts 9) or very little DNA polymerase (ts 11), at a non-permissive temperature, while ts 1, also DNA negative, induced a little more DNA polymerase than wild-type, often at both temperatures. The DNA polymerase induced by ts 6 at 31 degrees C was temperature-sensitive in vivo, but only slightly so in vitro. These results were confirmed immunologically and suggest that HSV-2 codes for at least part of a DNA polymerase activity, necessary for infection, and that full expression of this enzyme involves at least three viral genes.
J Gen Virol 1976 Apr
PMID:Herpesvirus proteins: DNA polymerase and pyrimidine deoxynucleoside kinase activities in temperature-sensitive mutants of herpes simplex virus type 2. 17 30

The R factor pMG2 protects Pseudomonas aeruginosa against the lethal effects of ultraviolet (u.v.) and gamma irradiation, and methyl methanesulphonate and N-methyl-N'-nitro-N-nitrosoguanidine treatment. Enhanced survival occurs in strains of uvr+ rec+ (wild-type) genotype and a variety of uvr rec+ type mutants. No protection occurs in a rec A-type mutant. The plasmid also enhances u.v.-induced mutagenesis. These effects appear to be due to host-cell controlled plasmid-determined DNA repair function(s). Studies on P. aeruginosa strains deficient in DNA polymerase I (polyA) suggest that a plasmid-determined repair resynthesis function may be responsible for increased u.v.-survival and enhanced u.v.-mutability in pMG2-containing bacteria.
J Gen Microbiol 1977 Jan
PMID:Plasmid modification of radiation and chemical-mutagen sensitivity in Pseudomonas aeruginosa. 18 73

Ultraviolet (u.v.) light-irradiation of human cytomegalovirus (HCMV) resulted in differential inactivation of virus capacities, e.g. induction of cell rounding, early antigens (EA), nuclear inclusion, HCMV DNA synthesis, cellular DNA synthesis, HCMV-specific DNA polymerase, cellular DNA polymerases and plaque production, while the capacity of HCMV to penetrate cell nuclei was not critically impaired. These results indicated that the virus-coded functions expressed after infection were responsible for sll these events except for HCMV-induced stimulation of cellular RNA synthesis which was enhanced by irradiation of the virus at a low dose of u.v. light (6600 ergs/mm2). In these experiments phosphonoacetic acid was effectively utilized to detect EA formation by immunofluorescent staining and to differentiate cellular DNA synthesis from virus DNA synthesis.
J Gen Virol 1978 Jan
PMID:Expression of early virus functions in human cytomegalovirus infected HEL cells: effect of ultraviolet light-irradiation of the virus. 20 66

Replication of herpes simplex virus type I (HSV-I) was studied in various cell lines of rat nervous system origin. Infection of neonatal rat glial primary cells with HSV-I, strain KOS, produced normal yields of progeny virus. Glioma lines B9 and B15 were permissive, the neuronal line B50 was partially restricted (10 to 100-fold reduction) and the neuronal line B103 was non-permissive (greater than 1000-fold reduction) for HSV-I (KOS) replication. Synthesis of virus DNA in infected B103 cells was not detected. However, at least some virus macromolecular synthesis was induced, including production of thymidine kinase, DNA polymerase and virus structural proteins.
J Gen Virol 1978 Apr
PMID:Infection by herpes simplex virus and cells of nervous system origin: characterization of a non-permissive interaction. 20 30

Ultraviolet irradiation of herpes simplex virus (HSV) did not affect the transfer of uncoated virus DNA to the nuclei of infected cells but the synthesis of virus DNA was suppressed. The virus-specific DNA polymerase was synthesized in cells infected with the u.v.-irradiated HF strain of HSV. In cells infected with the u.v.-irradiated KOS strain, the virus DNA polymerase activity was hardly detectable. The two strains of HSV differ in the sensitivity of the virus DNA polymerase gene to u.v.-irradiation.
J Gen Virol 1978 May
PMID:Interaction of ultraviolet-irradiated herpes simplex virus type 1 with BSC-1 cells. 20 61

Cells cultured from the breast muscles of 11 to 12-day-old chick embryos were infected in the undifferentiated mitotic myoblast stage or in the terminally differentiated non-mitotic myotube stage with one of two DNA viruses, vaccinia and herpes simplex virus type 1 (HSV-1). DNA synthesis was measured and production ov virus-specific DNA detected in cells infected as myoblasts or myotubes by isotope labelling, autoradiographic and buoyant density centrifugation techniques. Furthermore, fully fused myotubes resemble myoblasts in their ability to support productive infection by these DNA viruses although DNA replication and nuclear division have ceased in myotubes and only minimum levels of host-cell DNA polymerase activity are present.
J Gen Virol 1978 Dec
PMID:Replication of animal viruses in differentiating muscle cells: vaccinia and herpes simplex virus type 1. 21 53


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