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  • cellular
  • Nevertheless, inactivation of the catalytic or the DNA nick-binding functions of PARP affects cellular responses to genotoxins at the level of cell survival, sister chromatid exchanges and apoptosis [2, (springer.com)
  • distinct
  • Niewolik D, Vojtesek B, Kovarik J: p53-derived from human tumour cell lines and containing distinct point mutations can be activated to bind its consensus target sequence. (springer.com)
  • recruit
  • We propose that PARP-associated polymers may recruit signal proteins to sites of DNA breakage and reprogram their functions. (springer.com)
  • enzyme
  • Recent evidence obtained with transgenic knockout mice suggests that the enzyme poly(ADP-ribose)polymerase (PARP) does not play a direct role in DNA break processing [1, (springer.com)
  • polymerase
  • Schreiber V, Hunting D, Trueco C, Gowans B, Grunwald D, de Murcia G, Ménissier-de Murcia J: Dominant-negative mutant of human poly(ADP-ribose)polymerase affects cell recovery, apoptosis, and sister chromatid exchange following DNA damage. (springer.com)
  • Lindahl T, Satoh MS, Poirier GG, Klungland A: Posttranslational modification of poly(ADP-ribose)polymerase induced by DNA strand breaks. (springer.com)
  • Althaus FR: Role of poly(ADP-ribose)polymerase in base excision repair. (springer.com)
  • mice
  • PARP-deficient knockout mice from transgenic mice were found to exhibit several phenotypic features compatible with altered DNA damage signaling, such as downregulation and lack of responsiveness of p53 protein to genotoxins, and morphological changes compatible with MARCKS-related cytoskeletal dysfunction. (springer.com)
  • Wang ZQ, Auer B, Stingl L, Berghammer H, Haidacher D, Schweiger M, Wagner EF: Mice lacking ADPRT and poly(ADP-ribosyl)ation develop normally but are susceptible to skin disease. (springer.com)