The repair of endogenously and exogenously generated DNA modifications

Bernd Epe

Positions held

  • Since 2009: Chair of the Managing Council of the Institute of Pharmacy and Biochemistry, University of Mainz
  • 1994: Professor (C3) of Pharmacology and Toxicology at the Institute of Pharmacy in Mainz
  • 1989: Habilitation in Toxicology, Würzburg
  • 1983-1984: Academic Counsel and Outside Lecturer, Institute of Pharmacology and Toxicology, University of Würzburg
  • 1980-1983: Postdoc, MPI for Molecular Genetics, Berlin

Education

  • 1980: State Examination and Approbation as Pharmacist
  • 1977: PhD in Organic Chemistry, University Kiel
  • 1973: Diploma in Chemistry

Most relevant publications by Bernd Epe

Khobta A, Anderhub S, Kitsera N and Epe B (2010). Gene silencing induced by oxidative DNA base damage: association with local decrease of histone H4 acetylation in the promoter region. Nucleic Acids Res, 38, 4285-4295

Trapp C, Reite K, Klungland A and Epe B (2007). Deficiency of Cockayne Syndome B (CSB) gene aggrevates the genomic instability caused by endogenous oxidative DNA base damage in mice. Oncogene, 26, 4044-4048

Trapp C, Schwarz M and Epe B (2007). The peroxisome proliferator WY-14,643 promotes hepatocarcinogenesis caused by endogenously generated oxidative DNA base modifications in repair-deficient Csbm/m/Ogg1-/- mice. Cancer Res, 67, 5156-5161

Osterod M, Larsen E, Le Page F, Hengstler JG van der Horst GTJ, Boiteux S, Klungland A and Epe B (2002). A global DNA repair mechanism involving the Cockayne syndrome B (CSB) gene product can prevent the in vivo accumulation of endogenous oxidative DNA base damage. Oncogene, 21, 8232-8239

Klungland A, Rosewell I, Hollenbach S, Larsen E, Daly G, Epe B, Seeberg E, Lindahl T and Barnes DE (1999). Accumulation of pre-mutagenic DNA lesions in mice defective in removal of oxidative base damage. Proc Natl Acad Sci USA, 96, 13300-13305

  Research website