A role of the ERCC3 DNA helicase in DNA repair and apoptosis

Project leader: Miroslav Piršel
Project duration: 2007 - 2009

The initial reaction of a cell to DNA damage is to repair the damage. With increasing levels of DNA damage the cells switches to cell cycle arrest or to apoptosis. Apoptosis prevents clonal expansion of cells in which unrepaired damage would lead to mutation and to carcinogenesis. Cells that are defective in DNA repair tend to accumulate excess DNA damage. Cells defective in apoptosis tend to survive with excess DNA damage and thus allow DNA replication past DNA damages, causing mutations leading to carcinogenesis. DNA helicases are a highly conserved group of enzymes that unwind DNA and RNA. They function in all processes in which access to single-stranded DNA is required. ERCC3 helicase functions in nucleotide excision repair, transcription initiation and p53 dependent apoptosis. We intend to study a dual role of ERCC3 helicase in DNA repair and apoptosis in a unique set of hamster ERCC3 mutant cell lines.

Publications