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  • 1
    Electronic Resource
    Electronic Resource
    Hypoxia-selective antitumor agents. 2. Electronic effects of 4-substituents on the mechanisms of cytotoxicity and metabolic stability of nitracrine derivatives (1989)
    s.l. : American Chemical Society
    Journal of medicinal chemistry 32 (1989), S. 31-38 
    Details
    ISSN: 1520-4804
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/jm00121a007
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  • 2
    Electronic Resource
    Electronic Resource
    Human xeroderma pigmentosum group D gene encodes a DMA helicase (1993)
    [s.l.] : Nature Publishing Group
    Nature 365 (1993), S. 852-855 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] The XPD gene was expressed in yeast and XPD protein was purified to a very high degree (20,000 fold). Affinity-purified anti-XPD antibodies were used for immunoblotting to verify the expression of XPD protein in yeast and to monitor the elution of the protein from various chromatographic ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/365852a0
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  • 3
    Electronic Resource
    Electronic Resource
    Unraveling the Fanconi anemia–DNA repair connection (2005)
    [s.l.] : Nature Publishing Group
    Nature genetics 37 (2005), S. 921-922 
    Details
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Fanconi anemia is a chromosome instability disorder characterized by diverse congenital abnormalities, retarded growth, early predisposition to cancer and bone marrow failure. The hallmark of Fanconi anemia cells is their high sensitivity to chromosomal breakage and killing caused by exposure to ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/ng0905-921
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  • 4
    Electronic Resource
    Electronic Resource
    A CHO-cell mutant with a defect in cytokinesis (1976)
    Springer
    Somatic cell and molecular genetics 2 (1976), S. 387-400 
    Details
    ISSN: 1572-9931
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract In a selection procedure designed to enrich for temperature-sensitive mutant cells blocked in mitosis a CHO-cell mutant was isolated which has a defect in cytokinesis as the basis of its temperature-sensitive phenotype. Cultures of the mutant had an abnormally high percentage (ie, 34%) of polyploid cells at the permissive temperature of 34°C and showed further increased frequencies of polyploidy as well as many multinucleated cells at 38.5° and 39.5°. When the mutant cells were synchronized in metaphase by Colcemid arrest and then placed into fresh medium at nonpermissive temperature, they did not divide although the completion of mitosis appeared cytologically normal. Ultrastructural examination by electron microscopy of such synchronized cells at telophase revealed no specific defects in cellular components other than failure of development of a normal midbody. The sensitivity of the mutant to cytochalasin B and to Colcemid was the same as for wild-type cells. This mutation behaved as recessive in tetraploid cell hybrids constructed by fusing the mutant with a CHO strain which was wild-type with respect to temperature sensitivity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01542720
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  • 5
    Electronic Resource
    Electronic Resource
    Repair of DNA adducts in asynchronous CHO Cells and the role of repair in cell killing and mutation induction in synchronous cells treated with 7-bromomethylbenz[a]anthracene (1984)
    Springer
    Somatic cell and molecular genetics 10 (1984), S. 183-194 
    Details
    ISSN: 1572-9931
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract CHO cells of normal or UV-sensitive phenotypes were analyzed for their ability to remove DNA adducts produced by the carcinogen 7-BrMeBA. At a dose of 0.1 μM, which reduced the survival of the normal AA8 cells to ∼90 % and the mutant UV5 cells to ∼20%, the frequency of adducts was 5–6 per 106 nucleotides for both cell types, and AA8 cells removed ∼30% of the adducts in 8 h and ∼55% in 24 h. In contrast, UV5 and mutants from four other genetic complementation groups had no significant removal. Binding of 7-BrMeBA did not vary through the cell cycle in synchronous cultures. At a dose of mutagen (0.07 μM) resulting in ∼25% survival of asynchronous UV5, the survival of synchronous cultures rose about threefold from early G1 to early S phase and then decreased somewhat in late S/G2. At a dose (0.28 μM) producing similar survival of asynchronous cultures, AA8 cells differed qualitatively in that survival decreased progressively by 5-to 10-fold between early G1 and the early part of S, and rose steeply through late S/G2 to give a 10-to 20-fold increase. We conclude that DNA repair is the major determinant of variations in survival through the cycle in normal cells. The patterns observed are consistent with a mechanism of killing in AA8 cells in which adducts disrupt DNA replication, while in UV5 cells transcriptional blocks or other effects may govern lethality. Induced mutations at the aprt and hprt loci showed changes through the cycle in both AA8 and UV5 cells, and the patterns were not readily explainable by the action of repair.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01534907
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  • 6
    Electronic Resource
    Electronic Resource
    Different genetic alterations underlie dual hypersensitivity of CHO mutant UV-1 to DNA methylating and cross-linking agents (1985)
    Springer
    Somatic cell and molecular genetics 11 (1985), S. 523-532 
    Details
    ISSN: 1572-9931
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract CHO mutant UV-1, isolated on the basis of hypersensitivity to UV radiation (254 nm), was further characterized with respect to sensitivity to classes of DNA damaging agents in a differential cytotoxicity (DC) assay. Compared to its parental strain, Gly−A, UV-1 was dramatically (10-to 100-fold) hypersensitive to both DNA methylating and cross-linking agents. In addition, UV-1 was moderately (two- to fourfold) hypersensitive to several other classes of mutagens. DNA isolated from UV-1 or Gly− A after exposure to14C-labeled methylnitrosourea (MNU) contained similar amounts of label, thus ruling out differences in uptake or binding. Three phenotypic revertants of UV-1 were resistant to N-methyl-N′-nitro-N-nitrosoguanidine (MNNG) and other methylating agents but retained hypersensitivity to cross-linking agents. Moreover, fusion of UV-1 with two different UV-sensitive CHO mutants also having hypersensitivity to cross-link and methylation damage produced hybrids resistant to mitomycin C (MMC) but not to methyl methane sulfonate (MMS). Since the methylation and cross-link sensitivities were uncoupled in both genetic tests, the complex phenotype of UV-1 is likely due to more than one genetic alteration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01534718
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  • 7
    Electronic Resource
    Electronic Resource
    Effects of Ape1 Overexpression on Cellular Resistance to DNA-Damaging and Anticancer Agents (1999)
    Springer
    Somatic cell and molecular genetics 25 (1999), S. 253-262 
    Details
    ISSN: 1572-9931
    Keywords: Ape1 ; base excision repair ; cellular resistance ; L-OddC ; antimetabolite/nucleoside analog ; antiviral/anticancer agent
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract In vitro biochemical studies indicate that Ape1 is the major mammalian enzyme responsible for repairing abasic lesions in DNA and a significant factor in the processing of specific 3′-replication-blocking termini. Toward addressing the role of Ape1 in cellular resistance to specific DNA-damaging and anticancer agents, we constructed a chinese hamster ovary (CHO) cell line, AA8-Ape1, that exhibits a 7-fold higher Ape1-dependent nuclease activity; this overexpression is abolished upon exposure to tetracycline (Tc). In comparison to the AA8 parental control, our data indicates that Ape1 activity is not rate-limiting for the repair of cytotoxic damages induced by the alkylating agent methyl methanesulfonate (MMS), the oxidizing agent hydrogen peroxide (H2O2), or ionizing radiation (IR). AA8-Ape1 cells did exhibit increased resistance to bleomycin following a chronic 3-day exposure, but not to more acute challenges of 1 h. Most notably, the AA8-Ape1 line displayed ∼1.7-fold elevated resistance to the replication-blocking nucleoside analog dioxolane cytidine (L-OddC); this improved resistance was abrogated by the addition of Tc to the medium. These studies demonstrate that Ape1 is not rate-limiting in the repair of MMS- or H2O2-induced DNA damage, that Ape1 may dictate the sensitivity of bleomycin, depending on dosing scheme, and for the first time, that Ape1 can influence cellular resistance to the anticancer/antiviral antimetabolite L-OddC.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1019979613989
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  • 8
    Electronic Resource
    Electronic Resource
    Evidence for structural gene alterations affecting aminoacyl-tRNA synthetases in CHO cell mutants and revertants (1978)
    Springer
    Somatic cell and molecular genetics 4 (1978), S. 423-435 
    Details
    ISSN: 1572-9931
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Aminoacyl-tRNA synthetase (aaRS) activities in extracts of mutant strains of the Chinese hamster ovary line (CHO) were examined for alterations in thermal stability. Mutants having low activity for MetRS, AsnRS, or GlnRS contained aaRSs that were inactivated much more rapidly upon heating than those from wild-type cells. Revertant lines, isolated from cultures of these mutants (Asn-5, Met-2, and Gln-2) after treatment with nitrosoguanidine or ethyl methanesulfonate, had thermolabilities intermediate between mutant and wild-type, and consistently had higher activities than the mutants. With a modified in vivo aminoacylation procedure, two previously exceptional mutants, Arg-1 and His-1, showed pronounced reductions in the amount of arginyl-tRNA or histidyl-tRNA, respectively, under restrictive conditions, compared to wild type. Revertants of Arg-1 (like the mutant itself) had no measurable ArgRS in vitro activity (〈0.4% of wild type) although in vivo aminoacylation in the one revertant tested was partially restored. These data provide evidence that the forward mutations have occurred in the structural genes of the aaRSs and that most of the reversions are probably the result of second-site point mutations in the aaRS genes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01538864
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  • 9
    Electronic Resource
    Electronic Resource
    A screening method for isolating DNA repair-deficient mutants of CHO cells (1980)
    Springer
    Somatic cell and molecular genetics 6 (1980), S. 391-405 
    Details
    ISSN: 1572-9931
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract A simple procedure for isolating mutagen-sensitive clones of CHO cells was developed and applied in mutant hunts in which colonies were screened for hypersensitivity to killing by ultraviolet radiation (UV), ethyl methanesulfonate (EMS), or mitomycin C (MMC). Each of two UV-sensitive clones studied in detail had a D37 dose of 1.0 J/m2 compared to 7.0 J/m2 for the wild-type cells, and each was shown to have no detectable repair replication following exposure to UV doses of up to 26 J/m2. Although these mutants resemble xeroderma pigmentosum human mutants with respect to their repair defect and cross-sensitivity to the carcinogen 4-nitroquinoline-1-oxide, one of two clones (UV-20) is characterized by extreme hypersensitivity to MMC (80-fold as compared to the wild type). Clones having hypersensitivity to alkylating agents, but not UV, were obtained using MMC and EMS. In the latter case the two clones had significantly increased sensitivity to the killing action of60Co γ-rays.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01542791
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  • 10
    Electronic Resource
    Electronic Resource
    Hypersensitivity to mutation and sister-chromatid-exchange induction in CHO cell mutants defective in incising DNA containing UV lesions (1982)
    Springer
    Somatic cell and molecular genetics 8 (1982), S. 759-773 
    Details
    ISSN: 1572-9931
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Five UV-sensitive mutant strains of CHO cells representing different genetic complementation groups were analyzed for their ability to perform the incision step of nucleotide excision repair after UV exposure. The assay utilized inhibitors of DNA synthesis to accumulate the short-lived strand breaks resulting from repair incisions. After 6 J/m2, each of the mutants showed 〈10% of the incision rate of the parental AA8 cells. After 50 J/m2, the rate in AA8 was similar to that at 6 J/m2, but the rates in the mutants were significantly higher (∼20% of the rate of AA8). Thus by this incision assay the mutants were phenotypically indistinguishable. Each of the mutants were hypersensitive to mutation induction at both thehprt andaprt loci by a factor of 10, and in the one strain tested ouabain resistance was induced sevenfold more efficiently than in AA8 cells. Sister chromatid exchange was also induced with sevenfold increased efficiency in the two mutant strains examined. Thus, these CHO mutants resemble xeroderma pigmentosum cells in terms of their incision defects and their hypersensitivity to DNA damage by UV.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01543017
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