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  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of medicinal chemistry 34 (1991), S. 2414-2420 
    ISSN: 1520-4804
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Biochemical genetics 14 (1976), S. 611-617 
    ISSN: 1573-4927
    Keywords: Drosophila melanogaster ; phenol oxidases ; spectrophotometry ; electrophoresis ; suppression ; ribosomal proteins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract An interaction between the lozenge gene and the suppressor of forked gene of Drosophila melanogaster has been investigated both spectrophotometrically and electrophoretically. The nature of this interaction is such that certain lozenge alleles appear to be phenotypically suppressed while others are enhanced or unaffected, and the results reported demonstrate that the effect can clearly be observed at the biochemical level. Earlier observations have suggested that the suppressor of forked gene codes for a ribosomal protein, and this hypothesis is discussed.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Molecular genetics and genomics 188 (1982), S. 249-255 
    ISSN: 1617-4623
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Six recessive second chromosomal mutants of Drosophila melanogaster exhibiting larval hypersensitivity to methyl methanesulfonate have been identified and assigned to six complementation groups. The strains have been analyzed for their sensitivities to UV, X-ray, nitrogen mustard and formaldehyde. Two classes of mutants not previously observed in Drosophila have been identified. The mus 204A1 and mus 205A1 mutants exhibit sensitivity to MMS and UV but not X-ray or nitrogen mustard, while the mus 206A1 and mus 205A1 mutants display sensitivity to MMS, UV, and nitrogenmustard. Four of the seven strains exhibit poor female fertility and two of these are shown to have a weak meiotic disjunctional defect. Biochemical studies of the mus 205A1 mutant suggest a defect in DNA synthetic ability associated with excision and postreplication repair performed on UV and alkylation-damaged templates (Boyd and Harris 1981; Brown and Boyd 1981 b; R.L. Dusenbery, manuscript in preparation).
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1573-6822
    Keywords: ara-C ; dCTP pools ; DNA repair arrest ; XP-variant
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract DNA excision repair inhibition by arabinofuranosyl cytosine (ara-C) or by ara-C/hydroxyurea (HU) was measured in log phase and confluent cultures of normal and xeroderma pigmentosium (XP)-variant human fibroblasts following insult by ultraviolet (UV) light (20 J/m2). Repair inhibition was determined by measuring the accumulation of DNA single-strand breaks/108 daltons following cell culture exposure to ara-C or ara-C/HU in a series of 3 hr. pulses up ro 24 hr. after UV insult. Both normal and XP-variant derived cells showed a wide range of sensitivity to ara-C in log phase cells (0.2–9.4 breaks/108 daltons DNA), although strand break accumulation was constant for each specific cell line. The same cells were more sensitive to ara-C/HU with a 2–14 fold increase in DNA strand breaks depending upon the cell line assayed. In confluent cultures of normal cells, maximum sensitivity to ara-C and ara-C/HU was achieved with similar levels of repair inhibition observed (16.1 and 16.5 breaks/108 daltons, respectively). The same level of repair inhibition was observed in confulent XP-variants receiving ara-C/HU, but was reduced by 62–68% in cells treated with ara-C alone. Ara-C repair arrest was more rapidly reversed by competing concentrations of exogenous deoxycytidine (dCyd) in XP-variant compared to normal cells, especially in confluent cell cultures. In ara-C/HU treated cells, the level of dCyd reversal was reduced in the XP-variant when compared to cells exposed to ara-C alone. However, the same addition of HU had relatively little effect on dCyd reversal in normal cells. The measurements of dNTP levels indicate an elevated level of intracellular deoxycytosine triphosphate in XP-variant vs normal cells. The implications of these results are discussed as they relate to possible excision repair anomalies in the XP-variant.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1573-6822
    Keywords: DNA repair ; dNTPs ; ribonucleotide reductase inhibitors ; human fibroblasts
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Hydroxyurea, deoxyadenosine, pyridine-2-carboxaldehyde thiosemicarbazone, pyrazoloimidazole, 3,5-diamino-1,2,4 triazole (guanazole), 3,4,5-trihydroxy benzohydroxamic acid and 3,4-dihydroxy benzohydroxamic acid were examined for their effects on cellular dNTP pools, DNA excision repair, DNA replication and deoxynucleoside uptake in human diploid fibroblasts. All 7 agents were effective inhibitors of the UV excision repair process in noncycling quiescent cells, but not in rapidly dividing log-phase cells. This differential effect clearly demonstrates dependency upon modulation of cellular purine dNTP pool levels at the level of the reductase. Repair synthesis is shown to be less sensitive to all 7 reductase inhibitors than is replicative synthesis. Studies on cellular uptake of labeled DNA precursors in inhibitor-treated cells support the notion that deoxynucleosides cannot channel into the replicative synthesis process whereas they are readily utilized at repairing sites.
    Type of Medium: Electronic Resource
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