Yakubu Princely Abudu
Job description
Yakubu Princely Abudu is a Researcher in Molecular biology and Fluorescence nanoscopy. His research is focused on molecular and cellular mechanisms of selective autophagy and cell signaling and their interplay in neurodegenerative diseases and cancers. He is affiliated with the Autophagy Research Group, Department of Medical Biology and the Nanoscopy Group, Department of Physics and Technology, UiT-The Arctic University of Norway.
Biography
Yakubu obtained his bachelor’s degree from the University of Benin, Nigeria and post-graduate studies from the University of Tromsø, now UiT- The Arctic University of Norway. He obtained a master’s degree in Biomedicine in 2013 on 'studies of the subcellular distribution of human ATG8 family proteins and their role in autophagy' in the Molecular Cancer Research group, Department of Medical Biology, Faculty of Health Sciences, with Professor Terje Johansen as supervisor. He obtained his PhD in 2019 form the same group also with Terje Johansen as his supervisor. From 2019 to 2022, he was a postdoc on a grant from the Norwegian cancer society where he worked on the regulation of hypoxia signaling by selective autophagy. From 2022, he has been a senior researcher at the Nanoscopy Group, Department of Physics and Technology, studying how fluorescence Nanoscopy can be applied in basic medical research. From 2003, he has been a researcher at the Autophagy Research Group, Department of Medical Biology, University of Tromsø-The Arctic University of Norway, Tromsø, studying the molecular and cellular mechanisms of selective autophagy and its interplay in neurodegenerative diseases and cancers
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Research interests
Basic research into the molecular and cellular mechanisms of selective autophagy and cell signaling and how these affect neurodegenerative diseases and cancers. Cells remove damaged, worn-out or surplus proteins, lipids and organelles through selective autophagy. When this process goes wrong, it leads to conditions such as neurodegenerative diseases and cancers. The selective removal of damaged or surplus mitochondria through autophagy or mitophagy is crucial for maintaining cellular homeostasis and prevent diseases. We discovered that the proteins NIPSNAP1/2 act as ‘Eat-me’ signals on mitochondria that determine their removal. We have also discovered that the protein SAMM50 act as receptor to remove worn-out or surplus mitochondrial parts through piecemeal mitophagy.
Several drugs used to treat cancer tend to damage the mitochondria in other to induce apoptosis and kill cancer cells. We have now discovered that cancer cells are able to turn on mitophagy quickly to removed damaged mitochondrial upon treatment, and this process contribute greatly to drug resistance. We are now studying the mechanism of drug-induced mitophagy in other to understand how we can target this pathway to allow for cancer drugs to be more effective.
