- E-mailandreas.f.mathisen@uib.no
- Visitor AddressHaukeland universitetssykehus, Laboratoriebygget5009 Bergen
- Postal AddressPostboks 78045020 Bergen
Our research is directed at how cell death features (type, timing, extent) govern the type of regenerative strategy employed by a biological system.
We primarily use the murine pancreas as a model system, due to the wide-range of genetic tools available for this organ and its demonstrated cell plasticity potential. Besides employing classical systems of rapid cell-ablation (RIP-DTR, chemical ablation), we developed novel transgenic models of progressive β-cell decay (financed by Excellence Project for Young Investigators of Novo Nordisk Foundation). By coupling the diverse β-cell ablation configurations with genetic cell tracing, timed conditional gene expression and diverse omics assays, we study the dynamical molecular fingerprint of β-cell death and the regenerative response employed, with focus on β-cell self-renewal potential (financed by FRIPRO Young Research Talent grant – Research Council of Norway).
- (2023). Mapping islet architecture changes upon high fat diet challenge in a HNF1A-MODY mouse model.
- (2023). Islet maturation and ageing is governed by the Hnf1a transcription factor.
- (2023). Investigating the developmental role of HNF1A, HNF1B and HNF4A in human pancreatic islet cell differentiation.
- (2023). Human induced pluripotent stem cells as a model for environmental impact on diabetes.
- (2023). Hnf1a is a key regulator of β-cell identity and function.
- (2023). Hnf1a Is An Important Regulator in Ageing And Maturation Of Pancreatic Islets.
- (2023). Global proteomics reveals insulin abundance as a marker of human islet homeostasis alterations. Acta Physiologica. 15 pages.
- (2022). Molecular mechanisms affecting islet like cell fate acquisition in differentiating iPSC derived β-like cells”.
- (2022). Mind your background!
- (2022). Know your background, know your data.
- (2022). Hnf1a is a key regulator of β-cell identity and function.
- (2021). Chronically elevated exogenous glucose elicits antipodal effects on the proteome signature of differentiating human ipsc-derived pancreatic progenitors. International Journal of Molecular Sciences.
- (2020). In vivo environment swiftly restricts human pancreatic progenitors toward mono-hormonal identity via a HNF1A/HNF4A mechanism. Frontiers in Cell and Developmental Biology. 1-14.
- (2019). In vivo hyperglycemia exposure elicits distinct period-dependent effects on human pancreatic progenitor differentiation, conveyed by oxidative stress. Acta Physiologica. 1-16.
More information in national current research information system (CRIStin)