DNA repair and signaling in survival and death strategies of cells

Bernd Kaina

Positions held

  • 2004: Professor of Toxicology and Head of the Institute of Toxicology, University Medical Center, Mainz
  • 2003: Appointed Professor of Toxicology and Chair of General and Medical Toxicology at the Medical Center, University Göttingen, rejected
  • 1993: Professor of Toxicology and Head of the Division of Applied Toxicology at the Institute of Toxicology, Johannes Gutenberg University, Mainz
  • 1990: Habilitation, University Karlsruhe
  • 1987-1993: Group Leader at the Institute of Genetics and Toxicology, Kernforschungszentrum Karlsruhe and University of Karlsruhe
  • 1985-1987: Guest Researcher at the German Cancer Research Center, Department of Biochemistry, Heidelberg
  • 1984-1985: Grant Holder of the C.E.C. (Communities of European Countries) at the Laboratory of Molecular Genetics, State University of Leiden, The Netherlands
  • 1976-1984: Postdoc and Scientific Co-worker at the Central Institute of Genetics and Cultural Plant Breeding, Academy of Sciences of DDR, Gatersleben, East Germany

Education

  • 1977: PhD in Genetics, University Halle
  • 1975: Diploma in Biology, University Halle

Most relevant publications by Bernd Kaina

Roos WP, Jöst E, Belohlavek C, Nagel G, Fritz G and Kaina B (2011). Intrinsic anticancer drug resistance of malignant melanoma cells is abrogated by interferon-ß and valproic acid. Cancer Res, 15, 4150-4160

Wirtz S, Nagel G, Eshkind L, Neurath M, Samson LD and Kaina B (2010). Both base excision repair and O6- methylguanine-DNA methyltransferase protect against methylation-induced colon carcinogenesis. Carcinogenesis, 31, 2111-2117

Batista LFZ, Roos WP, Christmann M, Menck CFM and Kaina B (2007). Differential sensitivity of malignant glioma cells to methylating and chloroethylating anticancer drugs: p53 determines the switch by regulating xpc, ddb2 and DNA double-strand breaks. Cancer Res, 67, 11886-11895

Briegert M and Kaina B (2007). Human monocytes, but not dendritic cells derived from them, are defective in base excision repair and hypersensitive to methylating agents. Cancer Res, 67, 26-31

Roos WP, Christmann M, Fraser ST and Kaina B (2007). Mouse embryonic stem cells are hypersensitive to apoptosis triggered by the DNA damage O6-methylguanine due to high E2F1 regulated mismatch repair. Cell Death Diff, 14, 1422-1432

 

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