Helfrid Hochegger

Summary

Affiliation: Kyoto University
Country: Japan

Publications

  1. ncbi Multiple repair pathways mediate tolerance to chemotherapeutic cross-linking agents in vertebrate cells
    Kuniharu Nojima
    Department of Radiation Genetics, Kyoto University, Japan
    Cancer Res 65:11704-11. 2005
  2. ncbi Phenotypic analysis of cellular responses to DNA damage
    Helfrid Hochegger
    Dep. of Radiation Genetics, Graduate School Medicine, Kyoto University Sakyo-ku, Kyoto, Japan
    Subcell Biochem 40:313-25. 2006
  3. ncbi An essential role for Cdk1 in S phase control is revealed via chemical genetics in vertebrate cells
    Helfrid Hochegger
    Department of Radiation Genetics, Kyoto University Graduate School of Medicine, Kyoto, Japan
    J Cell Biol 178:257-68. 2007
  4. ncbi Parp-1 protects homologous recombination from interference by Ku and Ligase IV in vertebrate cells
    Helfrid Hochegger
    Department of Radiation Genetics, Faculty of Medicine, Kyoto University, Kyoto, Japan
    EMBO J 25:1305-14. 2006
  5. ncbi Inhibitors of the proteasome suppress homologous DNA recombination in mammalian cells
    Yasuhiro Murakawa
    Department of Radiation Genetics, Horizontal Medical Research Organization, Kyoto University Graduate School of Medicine, Kyoto, Japan
    Cancer Res 67:8536-43. 2007
  6. ncbi Critical roles for polymerase zeta in cellular tolerance to nitric oxide-induced DNA damage
    Xiaohua Wu
    Department of Radiation Genetics, Graduate School of Medicine, Kyoto University, Yoshida Konoe, Sakyo-ku, Kyoto 606-8501, Japan
    Cancer Res 66:748-54. 2006
  7. ncbi Fen-1 facilitates homologous recombination by removing divergent sequences at DNA break ends
    Koji Kikuchi
    Department of Radiation Genetics, Graduate School of Medicine, Kyoto University, Yoshidakonoe, Sakyo ku, Japan
    Mol Cell Biol 25:6948-55. 2005
  8. ncbi Vertebrate POLQ and POLbeta cooperate in base excision repair of oxidative DNA damage
    Michio Yoshimura
    Department of Radiation Genetics, CREST, Japan Science and Technology Laboratory, Graduate School of Medicine, Kyoto University, Yoshida Konoe, Sakyo ku, Kyoto 606 8501, Japan
    Mol Cell 24:115-25. 2006
  9. ncbi Extensive chromosomal breaks are induced by tamoxifen and estrogen in DNA repair-deficient cells
    Aki Mizutani
    Department of Radiation Genetics, Graduate School of Medicine, Kyoto University, Kyoto, Japan
    Cancer Res 64:3144-7. 2004
  10. ncbi Post-replication repair in DT40 cells: translesion polymerases versus recombinases
    Helfrid Hochegger
    Department of Radiation Genetics, Faculty of Medicine, Kyoto University, Sakyo-ku, 606-8501 Kyoto, Japan
    Bioessays 26:151-8. 2004

Collaborators

Detail Information

Publications13

  1. ncbi Multiple repair pathways mediate tolerance to chemotherapeutic cross-linking agents in vertebrate cells
    Kuniharu Nojima
    Department of Radiation Genetics, Kyoto University, Japan
    Cancer Res 65:11704-11. 2005
    ....
  2. ncbi Phenotypic analysis of cellular responses to DNA damage
    Helfrid Hochegger
    Dep. of Radiation Genetics, Graduate School Medicine, Kyoto University Sakyo-ku, Kyoto, Japan
    Subcell Biochem 40:313-25. 2006
    ..This review will give a brief overview of DNA double strand break repair, and will summarize phenotypes observed in DT40 mutants in these pathways, focusing on the methodological aspects of analysis...
  3. ncbi An essential role for Cdk1 in S phase control is revealed via chemical genetics in vertebrate cells
    Helfrid Hochegger
    Department of Radiation Genetics, Kyoto University Graduate School of Medicine, Kyoto, Japan
    J Cell Biol 178:257-68. 2007
    ..This study demonstrates essential functions of Cdk1 in the control of S phase, and exemplifies a chemical genetics approach to target cyclin-dependent kinases in vertebrate cells...
  4. ncbi Parp-1 protects homologous recombination from interference by Ku and Ligase IV in vertebrate cells
    Helfrid Hochegger
    Department of Radiation Genetics, Faculty of Medicine, Kyoto University, Kyoto, Japan
    EMBO J 25:1305-14. 2006
    ..Moreover, we found deletion of Ligase IV, another NHEJ gene, suppressed the camptothecin of PARP-1(-/-) cells. Our results suggest a new critical function for Parp in minimizing the suppressive effects of Ku and the NHEJ pathway on HR...
  5. ncbi Inhibitors of the proteasome suppress homologous DNA recombination in mammalian cells
    Yasuhiro Murakawa
    Department of Radiation Genetics, Horizontal Medical Research Organization, Kyoto University Graduate School of Medicine, Kyoto, Japan
    Cancer Res 67:8536-43. 2007
    ....
  6. ncbi Critical roles for polymerase zeta in cellular tolerance to nitric oxide-induced DNA damage
    Xiaohua Wu
    Department of Radiation Genetics, Graduate School of Medicine, Kyoto University, Yoshida Konoe, Sakyo-ku, Kyoto 606-8501, Japan
    Cancer Res 66:748-54. 2006
    ..The data reveal the critical role of TLS polymerases in cellular tolerance to NO-induced DNA damage and suggest the contribution of these error-prone polymerases to accumulation of single base substitutions...
  7. ncbi Fen-1 facilitates homologous recombination by removing divergent sequences at DNA break ends
    Koji Kikuchi
    Department of Radiation Genetics, Graduate School of Medicine, Kyoto University, Yoshidakonoe, Sakyo ku, Japan
    Mol Cell Biol 25:6948-55. 2005
    ..We conclude that Fen-1 eliminates heterologous sequences at DNA damage site and facilitates DNA repair by HR...
  8. ncbi Vertebrate POLQ and POLbeta cooperate in base excision repair of oxidative DNA damage
    Michio Yoshimura
    Department of Radiation Genetics, CREST, Japan Science and Technology Laboratory, Graduate School of Medicine, Kyoto University, Yoshida Konoe, Sakyo ku, Kyoto 606 8501, Japan
    Mol Cell 24:115-25. 2006
    ..Accordingly, POLQ and POLbeta share an overlapping function in the repair of oxidative base damage. Taken together, these results suggest a role for vertebrate POLQ in BER...
  9. ncbi Extensive chromosomal breaks are induced by tamoxifen and estrogen in DNA repair-deficient cells
    Aki Mizutani
    Department of Radiation Genetics, Graduate School of Medicine, Kyoto University, Kyoto, Japan
    Cancer Res 64:3144-7. 2004
    ..These data suggest a contribution of TLS to the prevention of chromosomal breaks by TAM and estrogen, and they therefore indicate that such error-prone DNA synthesis underlies mutagenesis induced by these agents...
  10. ncbi Post-replication repair in DT40 cells: translesion polymerases versus recombinases
    Helfrid Hochegger
    Department of Radiation Genetics, Faculty of Medicine, Kyoto University, Sakyo-ku, 606-8501 Kyoto, Japan
    Bioessays 26:151-8. 2004
    ..In this article, we aim to summarize our current understanding of post-replication repair in DT40 in the perspective of bacterial, yeast and mammalian genetics...
  11. ncbi Poly(ADP-ribose) polymerase 1 accelerates single-strand break repair in concert with poly(ADP-ribose) glycohydrolase
    Anna E O Fisher
    Genome Damage and Stability Centre, University of Sussex, Falmer, Brighton, United Kingdom
    Mol Cell Biol 27:5597-605. 2007
    ..Moreover, we identify PARG as a novel and critical component of SSBR that accelerates this process in concert with PARP-1...
  12. ncbi Reverse genetic studies of the DNA damage response in the chicken B lymphocyte line DT40
    Mitsuyoshi Yamazoe
    CRESTO, The Japan Science and Technology Corporation, Radiation Genetics, Graduate School of Medicine, Kyoto University, Yoshida Konoe, Sakyo-ku, Kyoto 606-8501, Japan
    DNA Repair (Amst) 3:1175-85. 2004
    ..This review summarizes the contribution of DT40 cells to reverse genetic studies of DNA damage response pathways in higher eukaryotic cells...
  13. ncbi RAD18 and poly(ADP-ribose) polymerase independently suppress the access of nonhomologous end joining to double-strand breaks and facilitate homologous recombination-mediated repair
    Alihossein Saberi
    CREST Research Project, Radiation Genetics, Faculty of Medicine, Kyoto University, Sakyo ku, Kyoto 606 8501, Japan
    Mol Cell Biol 27:2562-71. 2007
    ..In conclusion, higher-eukaryotic cells separately employ PARP1 and Rad18 to suppress the toxic effects of NHEJ during the HR reaction at stalled replication forks...