The Molecular Cancer Research Group performs basic research with a main focus on the molecular mechanims and roles of selective autophagy in cell signaling and disease mechanisms.
The macroautophagy process.
Following our discovery of the first mammalian selective autophagy receptors p62/SQSTM1 and NBR1 we have foccused our research on autophagy and particularly selective autophagy. Autophagy is an evolutionary conserved renovation process in cells, acting as a key regulator of cell survival or death in response to a variety of internal and external signals. Our work on the scaffold and signalling protein p62/SQSTM1 led to the discovery of autophagy receptors that specifically direct protein aggregates, organelles, nucleic acids and pathogens for degradation. Disabled autophagy plays a major role in human diseases including cancer, heart failure, metabolic, inflammatory and neurodegenerative diseases. Specific protein-protein interactions and their functional consequences are being addressed in all projects using a set of biochemical-, cell biological- and immunological tools. Bioimaging and Proteomics are important in the research strategy of the group. Our research is funded by the Norwegian Cancer Society and the Norwegian Research Council in addition to the support we receive from UiT.
-Our paper on NIPSNAP proteins as eat me signals for mitophagy of damaged mitochondria is now published Online now in Developmental Cell. The paper is the result of a collaboration between our group in Tromsø and Anne Simonsen's group in Oslo.
-New paper from Vojo Deretic's group with contributions from our group in Developmental Cell on phosphorylation of Syntaxin 17 by TBK1 controling initiation of autophagy.
-New paper in Autophagy in collaboration with Sharon Tooze group onm members of the autophagy class III phosphatidylinositol 3-kinase complex I interacting with GABARAP and GABARAPL1 via LIR motifs.
- New paper from our group in Journal of Cell Biology on a novel rapid autophagic degradation response to amino acid starvation which is indpendent of mTOR and degrades the selective autophagy receptors by endosomal micorautophagy.
-Paper from our group in EMBO Reports about FKBP8 as a novel mitophagy receptor.
- Paper in Nature on autophagy mediating degradation of nuclear lamina upon oncogene-induced senescence, with two members of our group as co-authors: