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)

Human cytomegalovirus (HCMV) infection of low serum-arrested confluent whole human embryo (Flow 5000) cells markedly stimulated ornithine decarboxylase (ODC) activity. Increased ODC activity was apparent by 12 h post-infection. The capacity of HCMV to stimulate ODC was: (1) dependent upon multiplicity of infection; (2) eliminated when the virus was neutralized with specific antiserum; and (3) sensitive to ultraviolet irradiation. Virus-mediated induction, in contrast to high serum induction of ODC, was not subject to inhibition by polyamines added to the growth medium. Phosphonoacetic acid (PAA) which blocks HCMV replication by inhibiting the activity of HCMV-specific DNA polymerase and which does not prevent HCMV induced stimulation of cell DNA synthesis, reversibly inhibited HCMV-induced stimulation of ODC activity by 74%. Studies with PAA indicated that HCMV-induced stimulation of ODC activity is independent of cell DNA synthesis and that the mechanism regulating virus-induced stimulation may be related to the HCMV-specific DNA polymerase.
J Gen Virol 1979 Feb
PMID:Stimulation of ornithine decarboxylase by human cytomegalovirus. 21 56

The phosphorylation of arabinofuranosylthymine (araThd) has been studied both in non-infected cells and in those infected with herpes simplex virus (HSV-1, Lennette; HSV-1, IES and HSV-2, D-316). In these experiments, HSV strains were used which either contain (Lennette, TK+ and D-316 TK+) or lack (IES, TK-) the capacity to induce pyrimidine deoxyribonucleoside kinase. It was found that extracellularly administered araThd is phosphorylated to ara TTP via araTMP and araTDP in both non-infected and in HSV-infected cells. The phosphorylating capacity is more than tenfold lower in non-infected cells than in infected cells. Interestingly, cells infected with the TK- strain have a tenfold higher phosphorylating capacity than normal, uninfected cells, a fact which might indicate that host cell deoxythymidine kinase is induced during HSV infection. AraTMP is incorporated into cellular DNA but not into HSV DNA. This finding is in contrast to observations with arabinofuranosyladenine, which is incorporated into both cellular and HSV DNA. In vitro experiments with HSV-induced DNA polymerase show that araTTP strongly inhibits the enzyme activity. Therefore we conclude that the inhibition of HSV DNA polymerase by araTTP (formed intracellularly from araThd) is the explanation for the observed antiviral activity of araThd.
J Gen Virol 1979 May
PMID:Phosphorylation of arabinofuranosylthymine in non-infected and herpesvirus (TK+ and TK-)-infected cells. 22 22

The present paper reports on the induction of two cell surface markers on human lymphoid cells following herpes simplex virus (HSV) infection. While both primary and chronic infections of human lymphoid cells led to the induction of receptors for the Fc region of 7S IgG, chronic HSV infection was also characterized by the induction of surface-bound IgM. Surface and intracellular Fc receptors were detected in the human lymphoid cell line, Raji, infected with HSV types 1 and 2. Under optimal conditions with a multiplicity of infection (m.o.i.) of 50 to 100 p.f.u. per cell, this marker was inducible in only about 53% of the infected cells. Kinetic studies revealed the appearance of these receptors at around 5 h following HSV infection and they reached a plateau 16 to 18 h p.i. Interestingly, this Fc receptor expression (i.e. percentage of positive cells) was found to be similar in primary and chronically HSV-infected Raji cells. Both human leukocyte interferon and phosphonoacetic acid (PAA), an inhibitor of herpesvirus DNA polymerase activity, effectively inhibited Fc receptor synthesis during primary HSV-infection and these two agents suppressed its induction in chronically HSV-infected Raji (Raji-HSV) cells. This inhibitory or suppressive effect, particularly of PAA, suggests that this HSV-induced Fc receptor may represent a late virus function in the infected cell. Unlike primary HSV infection, about 80% of the chronically HSV-infected Raji cells were found to express surface-bound IgM. This IgM induction was suppressed by long-term interferon treatment but not with PAA-treatment. Superinfection studies of interferon and PAA-treated Raji-HSV cells indicate that only the former would develop Fc receptors suggesting a protective role of this IgM against superinfection by HSV.
J Gen Virol 1979 Aug
PMID:Studies on the induction of IgG-Fc receptors and synthesis of IgM in primary and chronically-infected lymphoid (Raji) cells by herpes simplex virus. 23 Feb 88

The replication of the ColEl plasmid was studied in extracts from E. coli dnaG mutants. It was found that the synthesis of the complementary strands of ColEl DNA can be carried out in these extracts in two consecutive steps: (1) synthesis of the leading L strand independent of the dnaG function, and (2) synthesis of the lagging H strand depending upon addition of wild-type dnaG protein. In contrast to L strand synthesis, the latter reaction is insensitive to rifampicin and novobiocin. Both synthetic pathways are however blocked by antiserum directed against dnaB protein. This indicates an additional role of the dnaB protein in duplex DNA replication besides assisting the dnaG protein in the priming of lagging strand synthesis. The T7 gene-4 protein acting in conjunction with T7 DNA polymerase can substitute for both the function of the dnaB and dnaG protein. It is concluded that plasmid replication proceeds by a semi-discontinuous mechanism.
Mol Gen Genet 1979
PMID:Replication of the colicin E1 plasmid in extracts of Escherichia coli: uncoupling of leading strand from lagging strand synthesis. 23 24

Cleavage sites on the pWWO-8 plasmid were determined for the restriction endonucleases HindIII and XhoI. Terminal labelling using DNA polymerase I was particularly useful both for the characterisation of the smaller cleavage products and for confirmation of the order of fragments in the intact plasmid.
Mol Gen Genet 1979 Jan 05
PMID:An endonuclease cleavage map of the plasmid pWWO-8, a derivative of the TOL plasmid of Pseudomonas putida mt-2. 28 16

The effect of phage T4 gene 43 (DNA polymerase) mutations on recombination between adjacent base pairs was measured in rII amber and opal mutants. The mutator allele tsL56 did not promote recombination frequencies at the two sites in which its effect was studied. The antimutator allele tsCB87 caused slight or no reduction in recombination frequencies at five sites.
Mol Gen Genet 1979 Jan 11
PMID:Recombination in phage T4 gene-43 (DNA polymerase) mutants. 28 43

The ultraviolet (UV) sensitivity of Escherichia coli mutants deficient in the 5' leads to 3' exonuclease activity of DNA polymerase I is intermediate between that of pol+ strains and mutants which are deficient in the polymerizing activity of pol I (polA1). Like polA1 mutants, the 5'-exonclease deficient mutants exhibit increased UV-induced DNA degradation and increased repair synthesis compared to a pol+ strain, although the increase is not as great as in polA1 or in the conditionally lethal mutant BT4113ts deficient in both polymerase I activities. When dimer excision was measured at UV doses low enough to avoid interference from extensive DNA degradation, all three classes of polymerase I deficient mutants were found to remove dimers efficiently from their DNA. We conclude that enzymes alternative to polymerase I can operate in both the excision and resynthesis steps of excision repair and that substitution for either of the polymerase I functions results in longer patches of repair. A model is proposed detailing the possible events in the alternative pathways.
Mol Gen Genet 1977 Jan 07
PMID:Excision-repair in mutants of Escherichia coli deficient in DNA polymerase I and/or its associated 5' leads to 3' exonuclease. 31 38

Five mutants of Salmonella typhimurium strain LT2 trp DI (ColEI)+, initiallly detected because they released little or no colicin when tested on solid medium, proved to be sensitive to ultraviotet light (u.v.). Further testing indicated that one of the mutants was deficient in genetic recombination and was probably a recA-type mutant, while three of the others were deficient in DNA polymerase activity and appeared to be typical polA mutants. The fifth mutant was less sensitive than the others to methyl methanesulphonate, showed reduced proficiency in genetic recombination, and was of approximately normal u.v. mutability. This mutant may be a counterpart of the class known as uvrD in Escherichia coli. All five mutants degraded significantly more of their DNA following exposure to u.v. than did the wild-type strain. The recA-type mutant and the possible uvrD mutant also degraded significantly more of their DNA spontaneously than did the wild-type. Treatment with visible light and acridine orange (photodynamic treatment) cause no significant degradation of DNA in the wild-type strain, a highly significant increase in the extent of DNA degradation in a polA mutant, and a decrease in the extent of degradation in the recA-type mutant.
J Gen Microbiol 1977 Jul
PMID:DNA degradation in wild-type and repair-deficient strains of salmonella typhimurium exposed to ultraviolet light of photodynamic treatment. 33 Aug 21

The induction of prophage lambda by ultraviolet light has been measured in E. coli K12 lysogenic cells deficient in DNA polymerase I. The efficiency of the induction process was greater in polA1 polC(dnaE) double mutants incubated at the temperature that blocks DNA replication than in polA+ polC single mutants. Similarly, the polA1 mutation sensitized tif-promoted lysogenic induction in a polA1 tif strain at 42 degrees. In strains bearing the polA12 mutation, which growth normally at 30 degrees, induction of the prophage occurred after the shift to 42 degrees. It is concluded that dissapearance of the DNA polymerase I activity leads to changes in DNA replication that are able, per se, trigger the prophage induction process.
Mol Gen Genet 1977 Sep 09
PMID:Prophage induction in Escherichia coli K12 cells deficient in DNA polymerase I. 33 8

The mutation recL152 leads to a reduction of excision repair as measured by an increase in the time required to close uvrA uvrB dependent incision breaks, and by a reduction of host cell reactivation ability. Postreplication repair is also delayed when measured in a uvrB5 recL152 double mutant. Such a determination could not be made using the recL152 single mutant because the excision defect led to an accumulation of breaks in the unlabeled high molecular weight DNA to which the labeled DNA synthesized after irradiation must attach in order to achieve normal high molecular weight. Further, the recL gene product seems to be required to rejoin breaks in parental strand DNA which are generated during postreplication repair, since such gaps accumulate in a recL152 uvrB5 double mutant but not in a recL+ uvrB5 single mutant. We have noticed a striking phenotypic similarity between recL152 and polA1 and suggest that recL152 is required for full in vivo activity of DNA polymerase I.
Mol Gen Genet 1977 Oct 24
PMID:Defective excision and postreplication repair of UV-damaged DNA in a recL mutant strain of E. coli K-12. 34 Aug 83


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