Alterations in the levels of deoxyuridine triphosphatase, uracil-DNA glycosylase and AP endonuclease during the cell cycle

Duker, Nahum J.; Grant, Carol L.

doi:10.1016/0014-4827(80)90145-7

Cited by 51 publications

(25 citation statements)

References 15 publications

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“…However, this is not true for all the repair enzymes since the APendonuclease activity in dividing and undividing Chinese hamster cells remains unaltered [22]. Repair enzymes are probably either dependent or independent of DNA synthesis.…”

Section: Resultsmentioning

confidence: 98%

“…As to other repair enzymes it is known that phytohemagglutinin stimulation of lymphocytes increases repair synthesis g-fold after W-irradiation [20] and 20-fold after ionizing radiation [21]. However, this is not true for all the repair enzymes since the APendonuclease activity in dividing and undividing Chinese hamster cells remains unaltered [22]. Repair enzymes are probably either dependent or independent of DNA synthesis.…”

Section: Resultsmentioning

confidence: 99%

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Activity of uracil‐DNA glycosylase in different rat tissues and in regenerating rat liver

Aprelikova¹,

Tomilin²

1982

FEBS Letters

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Section: Resultsmentioning

confidence: 98%

Section: Resultsmentioning

confidence: 99%

Activity of uracil‐DNA glycosylase in different rat tissues and in regenerating rat liver

Aprelikova¹,

Tomilin²

1982

FEBS Letters

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“…Cellular dUTPases are ubiquitous enzymes which help to maintain a low ratio of dUTP to TTP and therefore minimize incorporation of uracil residues into DNA. They are regulated by the cell cycle, being at high levels in dividing, undifferentiated cells and at low levels in terminally differentiated, nondividing cells (4,17,21,25,31). A virally encoded dUTPase would presumably be advantageous for replication in nondividing cells like macrophages, which are the main target cells of ungulate lentiviruses in vivo and where the levels of endogenous dUTPase and the pool of deoxynucleotides are low (33).…”

mentioning

confidence: 99%

dUTPase-minus caprine arthritis-encephalitis virus is attenuated for pathogenesis and accumulates G-to-A substitutions

Turelli

Guiguen

Mornex

et al. 1997

J Virol

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The importance of the virally encoded dUTPase for CAEV replication, invasiveness, pathogenesis, and genetic stability was investigated in goats infected by viruses with single point (DU-G) and deletion (DU-1) mutations of the dUTPase gene (DU gene). The DU gene was found to be dispensable for CAEV replication in vivo as judged by times taken to seroconvert, frequencies of viral isolation, and tissue distribution of viral RNAs. DU ؊ reversion at week 34 in one of three goats infected with the single point mutant DU-G, however, suggested that the viral dUTPase confers some advantages for replication in vivo. Moreover, we show that dUTPase is necessary for the timely development of bilateral arthritic lesions of the carpus. Finally, dUTPase was shown to efficiently prevent accumulation of G-to-A transitions in the viral genome. Caprine arthritis-encephalitis virus (CAEV) (3) is a small

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“…Recent studies suggest that mammalian cells actively regulate each DNA repair pathway during the defined pattern of gene expression observed during cell proliferation (4,46). As compared with basal levels in quiescent cells, proliferating cells (a) have a greater capacity for DNA repair synthesis after exposure to ultraviolet irradiation (25,26,28,40,47,56), ionizing radiation (39), or alkylating agents (25,26,28,56); (b) have higher specific activities of the DNA repair enzymes uracil DNA glycosylase (1,10,19,23,58), 3-methyladenine DNA glycosylase (15,23), and the O6-methylguanine methyltransferase in the absence of cellular insult (49,50) or during toxicityinduced cellular hyperplasia (48); and (c) increase the rates of excision of DNA adducts as a function of their proliferative state (20,22,34).…”

mentioning

confidence: 99%

Regulation of DNA repair in serum-stimulated xeroderma pigmentosum cells.

Gupta¹,

Sirover²

1984

The Journal of Cell Biology

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The regulation of DNA repair during serum stimulation of quiescent cells was examined in normal human cells, in fibroblasts from three xeroderma pigmentosum complementation groups (A, C, and D), in xeroderma pigmentosum variant cells, and in ataxia telangiectasia cells. The regulation of nucleotide excision repair was examined by exposing cells to ultraviolet irradiation at discrete intervals after cell stimulation. Similarly, base excision repair was quantitated after exposure to methylmethane sulfonate. Wl-38 normal human diploid fibroblasts, xeroderma pigmentosum variant cells, as well as ataxia telangiectasia cells enhanced their capacity for both nucleotide excision repair and for base excision repair prior to their enhancement of DNA synthesis. Further, in each cell strain, the base excision repair enzyme uracil DNA glycosylase was increased prior to the induction of DNA polymerase using the identical cells to quantitate each activity. In contrast, each of the three xeroderma complementation groups that were examined failed to increase their capacity for nucleotide excision repair above basal levels at any interval examined. This result was observed using either unscheduled DNA synthesis in the presence of 10 mM hydroxyurea or using repair replication in the absence of hydroxyurea to quantitate DNA repair. However, each of the three complementation groups normally regulated the enhancement of base excision repair after methylmethane sulfonate exposure and each induced the uracil DNA glycosylase prior to DNA synthesis. These results suggest that there may be a relationship between the sensitivity of xeroderma pigmentosum cells from each complementation group to specific DNA damaging agents and their inability to regulate nucleotide excision repair during cell stimulation.Eucaryotic DNA repair pathways function to conserve the genetic information encoded in nucleotide sequences in cellular DNA. Two major excision repair pathways have been characterized in human cells. In nucleotide excision repair, which is responsible for the removal of pyrimidine dimers and other bulky lesions from DNA, the initial enzymatic action is endonucleolytic (29). Subsequently, the modified nucleotides are removed within an oligonucleotide fragment. In base excision repair, the initial enzymatic action is that of a DNA glycosylase (41). The glycosylase cleaves the base sugar glycosyl linkage removing the modified base and leaving an apurinic or apyrimidinic site in DNA. Recent studies suggest that mammalian cells actively regulate each DNA repair pathway during the defined pattern of gene expression observed during cell proliferation (4, 46). As compared with basal levels in quiescent cells, proliferating cells (a) have a greater capacity for DNA repair synthesis after exposure to ultraviolet irradiation (25,26,28, 40,47,56), ionizing radiation (39), or alkylating agents (25,26,28,56); (b) have higher specific activities of the DNA repair enzymes uracil DNA glycosylase (1,10,19,23,58),23), and the O6-methylguanine methylt...

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Alterations in the levels of deoxyuridine triphosphatase, uracil-DNA glycosylase and AP endonuclease during the cell cycle

Cited by 51 publications

References 15 publications

Activity of uracil‐DNA glycosylase in different rat tissues and in regenerating rat liver

Activity of uracil‐DNA glycosylase in different rat tissues and in regenerating rat liver

dUTPase-minus caprine arthritis-encephalitis virus is attenuated for pathogenesis and accumulates G-to-A substitutions

Regulation of DNA repair in serum-stimulated xeroderma pigmentosum cells.

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