Cancer starts with mutations in one cell or a small group of cells. Our ambition is to unveil the mechanisms leading to mutations.
Especially, we are interested in the analysis of the situation in cell cycle-arrested cells - since the major part of human somatic cell is in a non-replicating state. Due to numerous methodical advantages we use the yeast Saccharomyces cerevisiae as a model organism.
Novel double and single ryanodine receptor 1 variants in two Austrian malignant hyperthermia families
Kaufmann A, Kraft B, Michalek-Sauberer A, Weindlmayr M, Kress HG, Steinboeck F, Weigl LG.; Anesth Analg. 2012 May; 114(5):1017-25
The relevance of oxidative stress and cytotoxic DNA lesions for spontaneous mutagenesis in non-replicating yeast cellls
Steinboeck F, Hubmann M, Bogusch A, Dorninger P, Lengheimer T, Heidenreich E.;
Mutat Res. 2010 Jun 1; 688(1-2):47-52
A mutation-promotive role of nucleotide excision repair in cell cycle-arrested cell populations following UV irradiation
Heidenreich E, Eisler H, Lengheimer T, Dorninger P, Steinboeck F.;
DNA Repair (Amst). 2010 Jan 2; 9(1):96-100
The nuclear actin-related protein of Saccharomyces cerevisiae, Arp4, directly interacts with the histone acetyltransferase Esa1p
Steinboeck F, Bogusch A, Kaufmann A, Heidenreich E.;
J Biochem. 2007 May; 141(5):661-8
Novel regulatory properties of Saccharomyces cerevisiae Arp4
Steinboeck F, Krupanska L, Bogusch A, Kaufmann A, Heidenreich E.;
J Biochem. 2006 Apr; 139(4):741-51