Background and activities
Prof Magnar Bjørås is a Principle Investigator of the research group of Cellular responses to DNA damage at Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology (NTNU), Trondheim and at Oslo University Hospital/University of Oslo. Bjørås is an expert on genome dynamics with particular emphasis on oxidative stress, DNA base lesion repair and maintenance of epigenetic DNA methylation (epigenome stability).
Cellular genomes are continuously challenged by physical, chemical and biological agents that introduce changes of the chemical structure of the DNA. Intracellular reactive metabolites such as reactive oxygen species and alkylating compounds are important inducers of such changes. Nevertheless, mutation frequencies are low because of very efficient pathways for DNA repair and DNA recombination, which remove DNA damage and conserve at least one functional copy of the genome.
The main focus of the Bjørås group has been on repair of endogenous DNA base lesion repair mechanisms and genome stability. He has made major contributions to characterization of many new DNA repair enzymes from bacteria, yeast and mammalian (i.e. EMBO, 1990; Nature 1992; PNAS 1996; EMBO 1997; MCB 1997; NAR 2002; Nature 2002; JBC 2004; NAR 2005; Mol Micro 2006). He spent two years (2002-2004) in Professor John Tainer’s lab at Scripps Research Institute, California. His research group has solved the atomic structure (3D) of many DNA-protein complexes revealing several new mechanisms of DNA base damage recognition and catalysis (i.e. EMBO 2008; NSMB 2008; NSMB 2009; Cell Structure 2011; Cell Structure 2012; J Struct. Biol 2014). The last 10 years he has established research on the role of DNA base lesion repair in neurodegeneration, cognition and behavior, which is a new direction in the DNA repair field revealing novel functions beyond canonical DNA repair (i.e. Nature 2007; BMC Neurosci 2009; DNA repair 2008; Pediatric Res 2009; Brain Res 2010; Stem Cells 2010; J Neurosci 2011; PNAS 2011; Hum Mol Gen 2012; Cell Reports 2012; Cell Reports 2015). Bjørås has established collaborations with clinicians to study the impact of DNA base lesion repair on diseases such as infections (i.e Blood 2005; Virology 2006; JMB 2008 NAR 2008; PLoSOne 2010; PLoSGen, 2013, Int J Antimic Agents 2015), heart failure (Mutation Res 2009; J Mol Cell Card 2014; DNA repair 2015) metabolic diseases (Mol Genet Metab 2010; J Inherited Met Disease 2012 and 2013, Am J Hum Genet. 2014; Metabolism 2014) and cancer (Carcinogenesis 2009; Blood 2010; Blood 2012; DNA repair 2012).
Molecular mechanisms of DNA base lesion repair (Project leader: Magnar Bjørås)
Role of oxidative DNA base lesion repair in cancer (Project leader: Magnar Bjørås)
Impact of oxidative DNA base lesion repair and epigenetics on brain function (cognition, behavior and neurogenesis) (Project leaders: Magnar Bjørås and Katja Scheffler).
Small peptides in biological responses to DNA damage (Project leaders: Magnar Bjørås and James Booth).
Impact of Oxidation resistance gene 1 (Oxr1) in stress signaling (Project leader: Magnar Bjørås).
Scientific, academic and artistic work
A selection of recent journal publications, artistic productions, books, including book and report excerpts. See all publications in the database
- (2018) Novel activities of safe-in-human broad-spectrum antiviral agents. Antiviral Research. vol. 154.
- (2018) A systems approach to study immuno- and neuro-modulatory properties of antiviral agents. Viruses. vol. 10:423 (8).
- (2018) Excision of the doubly methylated base N4,5-dimethylcytosine from DNA by Escherichia coli Nei and Fpg proteins. Philosophical Transactions of the Royal Society of London. Biological Sciences. vol. 373 (1748).
- (2018) Increased nuclear DNA damage precedes mitochondrial dysfunction in peripheral blood mononuclear cells from Huntington's disease patients. Scientific Reports. vol. 8 (1).
- (2018) A transgenic minipig model of Huntington’s disease shows early signs of behavioral and molecular pathologies. Disease Models and Mechanisms. vol. 11 (10).
- (2018) Normal development of mice lacking PAXX, the paralogue of XRCC4 and XLF. FEBS Open Bio. vol. 8 (3).
- (2018) Ythdf2-mediated m6A mRNA clearance modulates neural development in mice. Genome Biology. vol. 19:69.
- (2018) Stress resilience of spermatozoa and blood mononuclear cells without prion protein. Frontiers in Molecular Biosciences. vol. 5:1.
- (2018) Neonatal Ogg1/Mutyh knockout mice have altered inflammatory gene response compared to wildtype mice in the brain and lung after hypoxia-reoxygenation. Journal of Perinatal Medicine.
- (2018) 8-oxoguanine DNA glycosylase (Ogg1) controls hepatic gluconeogenesis. DNA Repair. vol. 61.
- (2017) Integrative whole-genome sequence analysis reveals roles of regulatory mutations in BCL6 and BCL2 in follicular lymphoma. Scientific Reports. vol. 7 (1).
- (2017) Monitoring of the spatial and temporal dynamics of BER/SSBR pathway proteins, including MYH, UNG2, MPG, NTH1 and NEIL1-3, during DNA replication. Nucleic Acids Research. vol. 45 (14).
- (2017) Impaired oxidative stress response characterizes HUWE1-promoted X-linked intellectual disability. Scientific Reports. vol. 7:15050.
- (2017) Exercise induces cerebral VEGF and angiogenesis via the lactate receptor HCAR1. Nature Communications. vol. 8.
- (2017) NEIL3-Dependent Regulation of Cardiac Fibroblast Proliferation Prevents Myocardial Rupture. Cell reports. vol. 18.
- (2017) Glycosylated Chromogranin A in Heart Failure: Implications for Processing and Cardiomyocyte Calcium Homeostasis. Circulation: Heart Failure. vol. 10 (2).
- (2017) Metabolism and DNA repair shape a specific modification pattern in mitochondrial DNA. Mitochondrion (Amsterdam. Print). vol. 40.
- (2017) No cancer predisposition or increased spontaneous mutation frequencies in NEIL DNA glycosylases-deficient mice. Scientific Reports. vol. 7.
- (2017) Novel UCHL1 mutations reveal new insights into ubiquitin processing. Human Molecular Genetics. vol. 26 (6).
- (2017) Synthetic lethality between murine DNA repair factors XLF and DNA-PKcs is rescued by inactivation of Ku70. DNA Repair. vol. 57.