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)

DNA complementary to Nicotiana velutina mosaic virus (NVMV) RNA was cloned and five segments larger than 0.9 kb were used in Northern blot hybridization analysis to identify two virus-specific RNAs, approximately 8 kb (RNA 1) and 3 kb (RNA 2) in size. The clones selected as probes did not hybridize with RNA from various tobamoviruses, or from beet necrotic yellow vein (BNYVV) and peanut clump furoviruses. In an attempt to determine the taxonomic position of the virus, about 75% of the NVMV RNA 2 was sequenced and four open reading frames (ORFs) were identified. ORFs 1, 2 and 3 encode proteins of Mr 20K, 39K and 13K, whereas ORF 4 was incomplete. ORFs 2, 3 and 4 overlapped in an arrangement closely resembling the triple gene block identified in BNYVV RNA 2, barley stripe mosaic virus (BSMV) RNA 2, potato virus X and potato virus M RNA. The presumed coat protein gene of NVMV RNA 2 (ORF 1) is situated to the 5' side of the triple gene block as for BNYVV and BSMV RNA 2. Amino acid homologies were detected among the 13K and 14K proteins of NVMV RNA 2, BNYVV RNA 2 and BSMV RNA 2. Significant homology was also detected between the 39K protein of NVMV RNA 2 and the 42K protein of BNYVV RNA 2, with a motif specific for ATP- and GTP-binding (NTP-binding motif), and a conserved viral DNA polymerase domain. The presence of a triple gene block in NVMV RNA 2 indicates that NVMV has affinities with members of the hordei-, furo-, potex- and carlavirus groups but not with the tobamovirus group. The divided RNA genome of NVMV, and the sizes of the two RNAs suggest that NVMV is most closely allied to the furoviruses, but the unique nature of its different biological properties and lack of any serological relationships with furoviruses lead us to conclude that NVMV has no clear relatedness to any taxonomic group of plant viruses.
J Gen Virol 1990 May
PMID:Nicotiana velutina mosaic virus: evidence for a bipartite genome comprising 3 kb and 8 kb RNAs. 234 63

The replication of herpes simplex virus (HSV) type 1 in macrophages grown from spleen cells of mouse strains susceptible to HSV infection in vivo was very sensitive to interferon (IFN). Different types of mouse IFN (alpha, beta, gamma) exhibited similar antiviral activities. However, treatment of cells with IFN-gamma in combination with IFN-alpha or IFN-beta resulted in a synergistic inhibition of virus growth. As shown by assaying HSV DNA polymerase, IFN inhibited expression of the beta-genes. Inhibition of enzyme induction correlated well with the reduction of viral yield. Induction of HSV DNA polymerase was delayed by IFN in a dose-dependent manner. These results show that IFN inhibits HSV replication at an early step prior to or during the synthesis of beta-proteins.
J Gen Virol 1985 Oct
PMID:Inhibition of replication of herpes simplex virus in mouse macrophages by interferons. 241 65

Mutations which allow tolerance to 5-bromo-2'-deoxyuridine (BUdR) in a thymidine (TdR)-requiring strain of Bacillus subtilis have been examined. Differences in sensitivity to BUdR existed between isogenic strains harbouring the mutations. Those mutations originally isolated as BUdR-tolerant also bestowed tolerance to 5-bromouracil and vice versa. The strain exhibiting the greatest tolerance to BUdR maintained a normal rate of replication in the presence of BUdR whereas the parent strain did not, but the tolerant strain incorporated less analogue into DNA than the parent strain. The basis of the tolerance mutation appeared to lie at the point of uptake of the analogue into the cell as the tolerant mutant preferentially took up TdR over BUdR into whole cells. DNA polymerase activity measured in vitro did not distinguish between TdR and BUdR in either the parent or the mutant strain and although TdR kinase activity showed a preference for TdR over BUdR as a substrate, the extent of discrimination was similar in both strains.
J Gen Microbiol 1986 Feb
PMID:Tolerance to bromodeoxyuridine in a thymidine-requiring strain of Bacillus subtilis. 242 35

The RNA-dependent DNA polymerase (RDDP) of human immunodeficiency virus (HIV) was purified from sucrose density gradient-banded virus by four successive procedures: anion exchange chromatography, cation exchange chromatography, affinity chromatography on oligo(dT)-cellulose and adsorption chromatography on hydroxyapatite. The enzyme preparation was free of cellular DNA-dependent DNA polymerase activity. The properties of HIV RDDP were determined with a variety of template-primers. Generally, the enzyme used Mg2+ for optimal activity except with (Cm)n X (dG)12-18 as template-primer. Kinetic data (Michaelis constant, Hill coefficient) were calculated for several substrates.
J Gen Virol 1986 Dec
PMID:Functional purification and enzymic characterization of the RNA-dependent DNA polymerase of human immunodeficiency virus. 243 65

1. DNA repair was measured in 3 Gy gamma-irradiated human peripheral lymphocyte subpopulations by means of nucleoid sedimentation. 2. The influence of aphidicolin (an inhibitor of DNA polymerase) on the repair process was investigated. 3. Repair of 40-44% of the DNA lesions induced by gamma-irradiation was blocked by aphidicolin. 4. Enriched B- and T-lymphocyte fractions were affected by aphidicolin to the same extent.
Gen Pharmacol 1989
PMID:Aphidicolin inhibition of gamma-radiation-induced DNA repair in human lymphocyte subpopulations. 250 69

The dnaN and dnaQ genes encode the beta subunit and the epsilon subunit of the DNA polymerase III holoenzyme. Using translational fusions to lacZ we found that DNA damage caused by mitomycin C induces expression of the dnaA and dnaQ genes. This induction was not observed in lexA and recA mutants which block the induction of the SOS response, suggesting a relationship between the mechanism(s) of genetic control of DNA polymerase III holoenzyme and the SOS regulatory network. Nevertheless, there is evidence that the mitomycin C induction of dnaN and dnaQ is not a simple lexA-regulated process, because nalidixic acid (an excellent SOS inducer) does not increase dnaN and dnaQ gene expression, and the time course of induction is abnormally slow.
Mol Gen Genet 1989 Oct
PMID:Expression of the dnaN and dnaQ genes of Escherichia coli is inducible by mitomycin C. 251 28

The regulatory block P'R from the bacteriophage lambda has been inserted between the promoter and initial part of the gene into the plasmid pCJ55 carrying the gene for the Klenow fragment under the control of pL. As it should be predicted, at the inverted orientation the sharp decrease in the Klenow fragment quantity is registered. However, at the direct orientation there is some decrease in the synthesis of the protein, as compared with the synthesis of the Klenow fragment in the strain harbouring the plasmid pCJ55. A plausible explanation of the fact may be in the transcriptional interference of the promoters pL and p'R in artificially constructed structures.
Mol Gen Mikrobiol Virusol 1989 Feb
PMID:[Features of expression of cloned genes under the control of tandem promotors pL and pR of phage lambda]. 252 66

A series of herpes simplex virus isolates were recovered from a bone marrow transplant patient who received prolonged acyclovir therapy for indolent herpes simplex mouth and throat ulceration. Of 14 isolates received 10 were resistant to acyclovir and partially resistant to phosphonoacetic acid. Biochemical characterization revealed that resistance was due to an alteration in the virus DNA polymerase. DNA sequence analysis of the polymerase gene of a plaque-purified resistant virus isolate revealed a single nucleotide change when compared with the sequence of the gene of a plaque-purified sensitive isolate. This single base change resulted in a predicted amino acid substitution of Gly to Ser at residue number 841, a putative functional region of the polymerase.
J Gen Virol 1989 Feb
PMID:Characterization of a DNA polymerase mutant of herpes simplex virus from a severely immunocompromised patient receiving acyclovir. 254 43

Simian virus 40 (SV40) DNA, inserted into a plasmid vector, does not replicate when transfected into baby hamster kidney cells. However, when the recipient cells are superinfected with herpes simplex virus type 1 (HSV-1), extensive amplification of the introduced plasmid occurs. Deletion of the late SV40 region or part of the coding sequences of the small tumour (t) antigen has no effect on the efficiency of amplification, whereas manipulations affecting either the SV40 origin of replication or the integrity of large tumour (T) antigen substantially decrease HSV-induced amplification. Phosphonoacetic acid, an inhibitor of HSV DNA polymerase, strongly inhibits plasmid replication. Also, an HSV-1 mutant with a temperature-sensitive defect in the DNA polymerase gene (tsH) is unable to carry out amplification of test plasmids at the non-permissive temperature. On the other hand, a further mutant (tsS) causes SV40-plasmid amplification independent of the temperature, but this mutant fails to amplify a plasmid with an HSV origin at the non-permissive temperature. Thus, HSV-induced amplification of heterologous DNA is possible in the absence of HSV DNA replication. Since tsS putatively has a defect in the gene coding for an HSV origin-binding protein (UL9), this observation appears plausible. The implications for interaction between herpesviral replication functions and heterologous (possibly cellular) DNA sequences are discussed.
J Gen Virol 1989 Jun
PMID:Herpes simplex virus causes amplification of recombinant plasmids containing simian virus 40 sequences. 254 82

An insertion mutant of herpes simplex virus type 1 has been constructed which carries the lacZ gene from Escherichia coli within the coding sequence of gene UL2, which is in the long unique region of the genome. In a one-step growth curve experiment this recombinant (called in 1601) grew as well as the wild-type (wt) parent virus, indicating that the UL2 gene is dispensable for growth in tissue culture. Analysis of in 1601 DNA with restriction endonucleases showed no detectable changes from the wt apart from the insertion. Extracts of cells infected with in 1601 possessed levels of viral DNA polymerase and alkaline exonuclease activities similar to those infected with the wt, but unlike the wt had negligible uracil-DNA glycosylase activity, suggesting strongly that the product of the UL2 gene is the uracil-DNA glycosylase. The sequence of the uracil-DNA glycosylase gene of E. coli was recently published, and the encoded amino acid sequence of this shows clear similarity to that of UL2, confirming our results.
J Gen Virol 1989 Feb
PMID:Gene UL2 of herpes simplex virus type 1 encodes a uracil-DNA glycosylase. 256 40


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