Yakubu Princely Abudu
Job description
Yakubu Princely Abudu is a researcher and project leader specializing in molecular biology, selective autophagy, cell signaling, and fluorescence nanoscopy. He is affiliated with the Autophagy Research Group in the Department of Medical Biology and the Nanoscopy Group in the Department of Physics and Technology at UiT The Arctic University of Norway.
His research focuses on the molecular and cellular mechanisms that regulate selective autophagy and how these processes interact with cell-signaling pathways. He investigates how defects in cellular quality-control systems contribute to the development and progression of neurodegenerative diseases and cancer.
As a project leader, he oversees research projects involving advanced imaging technologies, including fluorescence nanoscopy, to examine cellular processes at high spatial and molecular resolution. He is also the project leader of REMTSA, a research project investigating the regulation of epithelial-to-mesenchymal transition (EMT) by selective autophagy in breast cancer
Biography
Yakubu Princely Abudu is a researcher and project leader at the Faculty of Health Sciences, UiT The Arctic University of Norway. His work lies at the intersection of molecular biology, cell signaling, autophagy, cancer biology, and advanced fluorescence imaging.
He completed his postgraduate studies at the University of Tromsø, now UiT The Arctic University of Norway. He obtained a master’s degree in Biomedicine for research on the subcellular distribution of human ATG8-family proteins and their role in autophagy. His master’s research was conducted in the Molecular Cancer Research Group, Department of Medical Biology, Faculty of Health Sciences, under the supervision of Professor Terje Johansen.
He completed his PhD in the same research group, also under the supervision of Professor Terje Johansen. He subsequently worked as a postdoctoral fellow, studying the regulation of hypoxia signaling by selective autophagy.
Abudu later served as a senior researcher in the Nanoscopy Group, Department of Physics and Technology, where he investigated the application of fluorescence nanoscopy to basic medical research. He is currently a researcher in the Autophagy Research Group, Department of Medical Biology, at UiT, where he studies the molecular and cellular mechanisms of selective autophagy and their relevance to neurodegenerative diseases and cancer.
He is the project leader of REMTSA, a research project focused on studying the regulation of epithelial-to-mesenchymal transition (EMT) by selective autophagy in breast cancer.
The 50 latest publications is shown on this page. See all publications in NVA here →
Research interests
My research focuses on the molecular and cellular mechanisms of selective autophagy, mitophagy, and cell signaling, and how defects in these processes contribute to neurodegenerative diseases and cancer. Selective autophagy is a cellular quality-control system that removes damaged, surplus, or unwanted proteins, lipids, and organelles. By maintaining cellular homeostasis, this process is essential for healthy cell function. When autophagy is impaired or dysregulated, it can contribute to diseases including Parkinson’s disease, other neurodegenerative disorders, and cancer.
A major focus of my research has been mitophagy, the selective removal of damaged or surplus mitochondria. Mitochondria are essential for energy production and cellular signaling, but damaged mitochondria can generate harmful stress and contribute to neuronal dysfunction. Understanding how cells identify and eliminate defective mitochondria is therefore particularly important for understanding Parkinson’s disease and other neurodegenerative conditions.
My work contributed to the discovery that NIPSNAP1 and NIPSNAP2 function as “eat-me” signals on damaged mitochondria. These proteins help mark mitochondria for recognition by autophagy receptors and support the sustained recruitment of the autophagy machinery during mitophagy. I have also contributed to the discovery that SAMM50 acts as a receptor in piecemeal mitophagy, a process that enables cells to selectively remove damaged or surplus components of mitochondria rather than eliminating the entire organelle. These findings have advanced our understanding of how mitochondrial quality control is regulated and how its failure may contribute to neurodegenerative disease.
My research has also examined the regulation of autophagy through signaling pathways and autophagy receptors. This includes work on TBK1-dependent signaling, ATG8-family proteins, SNARE proteins, lysosomal damage, mTOR regulation, and the molecular mechanisms that control the initiation and selectivity of autophagy. In addition, my research has contributed to the broader development and interpretation of experimental methods used to monitor autophagy.
Another important area of my work concerns the relationship between mitophagy and cancer treatment. Many anticancer drugs damage mitochondria to induce apoptosis and eliminate cancer cells. However, cancer cells can rapidly activate mitophagy to remove drug-damaged mitochondria. This protective response can help cancer cells survive treatment and may contribute to drug resistance. My current research in this area investigates the mechanisms of drug-induced mitophagy and seeks to determine whether this pathway can be targeted to improve the effectiveness of cancer therapies.
My current work also focuses on epithelial-to-mesenchymal transition (EMT) in breast cancer. EMT is a cellular process associated with changes in cell identity, migration, invasion, metastasis, and treatment response. As project leader, I am investigating the molecular and cellular mechanisms that regulate EMT and how these processes interact with autophagy, mitochondrial quality control, and cell signaling. This research aims to improve our understanding of breast cancer progression and identify potential strategies for making cancer treatment more effective.
Across these research areas, I combine molecular and cellular biology with advanced imaging approaches, including fluorescence nanoscopy. This interdisciplinary approach allows me to investigate autophagy, mitophagy, mitochondrial dynamics, and cancer-associated cell signaling with high spatial and molecular resolution. Overall, my research seeks to explain how cells maintain quality control, how these systems become disrupted in disease, and how they can be therapeutically targeted in neurodegenerative diseases and cancer.
Teaching
FYS-8805-Cell Culture and Labelling
