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
- (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) Glycosyalted chromogranin A in heart faiure. Implications for processing and cardiomyocyte calcium homeostasis. Circulation: Heart Failure. vol. 10:e003675 (2).
- (2017) No cancer predisposition or increased spontaneous mutation frequencies in NEIL DNA glycosylases-deficient mice. Scientific Reports. vol. 7 (1).
- (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.
- (2016) N-Acetylcysteine Amide Exerts Possible Neuroprotective Effects in Newborn Pigs after Perinatal Asphyxia. Neonatology. vol. 111 (1).
- (2016) Broad histone H3K4me3 domains in mouse oocytes modulate maternal-to-zygotic transition. Nature. vol. 537 (7621).
- (2016) Neil3 induced neurogenesis protects against prion disease during the clinical phase. Scientific Reports. vol. 6.
- (2016) Mutually exclusive RNA secondary structures regulate translation initiation of DinQ in Escherichia coli. RNA: A publication of the RNA Society. vol. 22 (11).
- (2016) Regulation of Human Endonuclease V Activity and Relocalization to Cytoplasmic Stress Granules. Journal of Biological Chemistry. vol. 291.
- (2016) Crystal structure and MD simulation of mouse EndoV reveal wedge motif plasticity in this inosine-specific endonuclease. Scientific Reports. vol. 6.
- (2016) PML regulates neuroprotective innate immunity and neuroblast commitment in a hypoxic–ischemic encephalopathy model. Cell Death & Disease. vol. 7.
- (2016) Efficient and Reliable Production of Vectors for the Study of the Repair, Mutagenesis, and Phenotypic Consequences of Defined DNA Damage Lesions in Mammalian Cells. PLoS ONE. vol. 11 (6).
- (2016) 3CAPS - A structural AP-site analogue as a tool to investigate DNA base excision repair. Nucleic Acids Research. vol. 44 (5).
- (2016) Enhanced base excision repair capacity in carotid atherosclerosis may protect nuclear DNA but not mitochondrial DNA. Free Radical Biology & Medicine. vol. 97.
- (2016) Neil3-dependent base excision repair regulates lipid metabolism and prevents atherosclerosis in Apoe-deficient mice. Scientific Reports. vol. 6:28337.