NOVEL CHINESE-HAMSTER ULTRAVIOLET-SENSITIVE MUTANTS FOR EXCISION REPAIR FORM COMPLEMENTATION GROUP-9 AND GROUP-10 (Articolo in rivista)

Type
Label
  • NOVEL CHINESE-HAMSTER ULTRAVIOLET-SENSITIVE MUTANTS FOR EXCISION REPAIR FORM COMPLEMENTATION GROUP-9 AND GROUP-10 (Articolo in rivista) (literal)
Anno
  • 1991-01-01T00:00:00+01:00 (literal)
Alternative label
  • Stefanini M, Collins A, Riboni R, Klaude M, Botta E, Mitchell DL and Nuzzo F (1991)
    NOVEL CHINESE-HAMSTER ULTRAVIOLET-SENSITIVE MUTANTS FOR EXCISION REPAIR FORM COMPLEMENTATION GROUP-9 AND GROUP-10
    in Cancer research (Chic. Ill.); American association for cancer research, Philadelphia [Pa.] (Stati Uniti d'America)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Stefanini M, Collins A, Riboni R, Klaude M, Botta E, Mitchell DL and Nuzzo F (literal)
Pagina inizio
  • 3965 (literal)
Pagina fine
  • 3971 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 51 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
  • 15 (literal)
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Stefanini, Riboni, Botta, Nuzzo: IGBE CNR Pavia Collins, Klaude: Dept Mol Cell Biology, University of Aberdeen, Aberdeen, Scotland Mitchell: Lab Radiobiology Environmental Health, University of California, San Francisco, CA (literal)
Titolo
  • NOVEL CHINESE-HAMSTER ULTRAVIOLET-SENSITIVE MUTANTS FOR EXCISION REPAIR FORM COMPLEMENTATION GROUP-9 AND GROUP-10 (literal)
Abstract
  • In this paper we demonstrate that the mutants CHO7PV and CHO4PV isolated by us from the CHO-K1 prol- cell line represent two new complementation groups of UV-sensitive excision repair-defective rodent mutants. We have classified the mutant CH07PV as representative of Group 9 and CHO4PV as representative of Group 10. Cellular and biochemical characterization of these mutants indicates that they are moderately sensitive to a broad spectrum of mutagens (UV and mono- and bifunctional alkylating agents), partially unable to perform UV-induced DNA repair synthesis, and partially defective in the incision step of the DNA excision repair pathway and in the removal of the two main lesions caused by UV [cyclobutane pyrimidine dimers and (6-4) photoproducts]. In terms of UV survival and incision, CHO4PV is apparently more defective than CHO7PV (40% and 50% of wild-type survival, respectively, and 55% and 75% of wild-type incision), whereas when repair DNA synthesis and lesion removal are compared, CHO7PV seems to be more severely affected (30% of wild-type unscheduled DNA synthesis in CHO7PV and 60% in CHO4PV). This suggests a subtlety in the relation between removal of these specific lesions and overall repair capacity and survival. (literal)
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