Bilde av Abudu, Yakubu Princely
Bilde av Abudu, Yakubu Princely
Researcher / Autophagy Research Group Autophagy Research Group yakubu.p.abudu@uit.no You can find me here

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, Norway.


  • Athanasios Kournoutis, Trond Lamark, Terje Johansen, Yakubu Princely Abudu :
    WDR83/MORG1 inhibits RRAG GTPase-MTORC1 signaling to facilitate basal autophagy
    Autophagy 2024 ARKIV / DOI
  • Yakubu Princely Abudu, Athanasios Kournoutis, Hanne Britt Brenne, Trond Lamark, Terje Johansen :
    MORG1 limits mTORC1 signaling by inhibiting Rag GTPases
    Molecular Cell 2024 ARKIV / DOI
  • Jianwen Zhou, Nikoline Lander Rasmussen, Hallvard Lauritz Olsvik, Vyacheslav Akimov, Zehan Hu, Gry Evjen et al.:
    TBK1 phosphorylation activates LIR-dependent degradation of the inflammation repressor TNIP1
    Journal of Cell Biology 2023 ARKIV / DOI
  • Juncal Garcia Garcia, Anne Kristin McLaren Berge, Katrine Stange Overå, Kenneth Bowitz Larsen, Zambarlal Babanrao Bhujabal, Andreas Brech et al.:
    TRIM27 is an autophagy substrate facilitating mitochondria clustering and mitophagy via phosphorylated TBK1
    The FEBS Journal 2022 ARKIV / DOI
  • Martina Wirth, Stephane Mouilleron, Wenxin Zhang, Eva Sjøttem, Yakubu Princely Abudu, Ashish Jain et al.:
    Phosphorylation of the LIR Domain of SCOC Modulates ATG8 Binding Affinity and Specificity
    Journal of Molecular Biology (JMB) 2021 ARKIV / DOI
  • Daniel J. Klionsky, Amal Kamal Abdel-Aziz, Sara Abdelfatah, Mahmoud Khaled Abdellatif, Asghar Abdoli, Yakubu Princely Abudu et al.:
    Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)
    Autophagy 2021 DOI
  • Yakubu Princely Abudu, Stephane Mouilleron, Sharon A Tooze, Trond Lamark, Terje Johansen :
    SAMM50 is a receptor for basal piecemeal mitophagy and acts with SQSTM1/p62 in OXPHOS-induced mitophagy
    Autophagy 2021 ARKIV / DOI
  • Yakubu Princely Abudu, Birendra Kumar Shrestha, Wenxin Zhang, Anthimi Palara, Hanne Britt Brenne, Kenneth Bowitz Larsen et al.:
    SAMM50 acts with p62 in piecemeal basal- and OXPHOS-induced mitophagy of SAM and MICOS components
    Journal of Cell Biology 2021 ARKIV / DOI
  • Suresh Kumar, Yuexi Gu, Yakubu Princely Abudu, Jack-Ansgar Bruun, Ashish Jain, Farzin Farzam et al.:
    Phosphorylation of Syntaxin 17 by TBK1 Controls Autophagy Initiation
    Developmental Cell 28. April 2019 ARKIV / DOI
  • Yakubu Princely Abudu, Serhiy Pankiv, Benan John Mathai, Alf Håkon Lystad, Christian Bindesbøll, Hanne Britt Brenne et al.:
    NIPSNAP1 and NIPSNAP2 act as “eat-me signal” for mitophagy
    Developmental Cell 11. April 2019 ARKIV / DOI
  • Birendra Kumar Shrestha, Mads Skytte Rasmussen, Yakubu Princely Abudu, Jack-Ansgar Bruun, Kenneth Bowitz Larsen, Endalkachew Ashenafi Alemu et al.:
    NIMA-related kinase 9–mediated phosphorylation of the microtubule-associated LC3B protein at Thr-50 suppresses selective autophagy of p62/sequestosome 1
    Journal of Biological Chemistry 2019 ARKIV / DOI
  • Yakubu Princely Abudu, Serhiy Pankiv, Benan John Mathai, Trond Lamark, Terje Johansen, Anne Simonsen :
    NIPSNAP1 and NIPSNAP2 act as “eat me” signals to allow sustained recruitment of autophagy receptors during mitophagy
    Autophagy 2019 DOI
  • Aurélien Schwob, Elodie Teruel, Louise Dubuisson, Florence Lormières, Pauline Verlhac, Yakubu Princely Abudu et al.:
    SQSTM-1/p62 potentiates HTLV-1 Tax-mediated NF-κB activation through its ubiquitin binding function
    Scientific Reports 05. November 2019 ARKIV / DOI
  • Yuexi Gu, Yakubu Princely Abudu, Suresh Kumar, Bhawana Bissa, Seong Won Choi, Jingyue Jia et al.:
    Mammalian Atg8 proteins regulate lysosome and autolysosome biogenesis through SNAREs
    EMBO Journal 18. October 2019 ARKIV / DOI
  • Jakob Mejlvang, Hallvard Lauritz Olsvik, Steingrim Svenning, Jack-Ansgar Bruun, Yakubu Princely Abudu, Kenneth Bowitz Larsen et al.:
    Starvation induces rapid degradation of selective autophagy receptors by endosomal microautophagy
    Journal of Cell Biology 17. July 2018 ARKIV / DOI
  • Jingyue Jia, Yakubu Princely Abudu, Aurore Claude-Taupin, Yuexi Gu, Suresh Kumar, Seong Won Choi et al.:
    Galectins Control MTOR and AMPK in Response to Lysosomal Damage to Induce Autophagy
    Autophagy 06. August 2018 DOI
  • Jingyue Jia, Yakubu Princely Abudu, Aurore Claude-Taupin, Yuexi Gu, Suresh Kumar, Seong Won Choi et al.:
    Galectins Control mTOR in Response to Endomembrane Damage
    Molecular Cell 2018 DOI
  • Mads Skytte Rasmussen, Stephane Mouilleron, Birendra Kumar Shrestha, Martina Wirth, Rebecca Lee, Kenneth Bowitz Larsen et al.:
    ATG4B contains a C-terminal LIR motif important for binding and efficient cleavage of mammalian orthologs of yeast Atg8
    Autophagy 2017 DOI
  • Martina Wirth, Stephane Mouilleron, Wenxin Zhang, Eva Sjøttem, Yakubu Princely Abudu, Ashish Jain et al.:
    Corrigendum to Phosphorylation of the LIR Domain of SCOC Modulates ATG8 Binding Affinity and Specificity (Journal of Molecular Biology (2021) 433(13), (S0022283621001881), (10.1016/j.jmb.2021.166987))
    Journal of Molecular Biology (JMB) 2021 DOI
  • Hallvard Lauritz Olsvik, Steingrim Svenning, Yakubu Princely Abudu, Andreas Brech, Harald Stenmark, Terje Johansen et al.:
    Endosomal microautophagy is an integrated part of the autophagic response to amino acid starvation
    Autophagy 2018 DOI

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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.


    Member of research group