Maaike Tierie PhD student
Contact
Name and title: Maaike TieriePhD student
Workplace: Department of Biochemistry and Biophysics Länk till annan webbplats.
Visiting address Room M446Svante Arrhenius väg 16
Postal address Institutionen för biokemi och biofysik106 91 Stockholm
Unravelling the regulation and functions of Fe65
My main goal is to help provide a better understanding of the molecular mechanisms underlying neurodegenerative diseases, such as Alzheimer’s disease and amyotrophic lateral sclerosis (ALS). The focus is, in particular, on a protein called Fe65, which is interesting because it can interact with many different partners. Among these are tau and APP, two proteins that are altered in Alzheimer’s disease.
Through its many interactions, Fe65 forms different complexes that appear in distinct parts of the cell, both the cytoplasm and the nucleus. Because of these different locations and partners, Fe65 has been linked to a wide range of biological processes, from DNA repair and gene regulation to maintaining cell structure and transporting materials inside the cell. Together, these findings strengthen the idea that Fe65 may play important roles in biological processes known to be dysregulated in neurodegenerative disease. However, much about this protein remains unknown, both under normal physiological conditions and in the context of neurodegenerative diseases.
To address these gaps, cellular models will be used in combination with molecular and biochemical techniques to answer questions such as:
- How are Fe65’s interactions and its localisation inside the cell regulated? How do post‑translational modifications influence this regulation?
- What different Fe65 complexes exist? What functions do they perform, and are these complexes altered under neurodegenerative conditions?
- How does Fe65 interact with tau? How is this interaction regulated, what is its function, and does it differ depending on the forms or modifications of the proteins? Is this interaction impaired in Alzheimer’s disease or other tau‑related disorders?
- What is Fe65’s role at the neuromuscular junction (NMJ)? Loss of either APP or Fe65 disrupts NMJ function, a hallmark of ALS. What is the role of Fe65 and Fe65-interacting partners at the NMJ, and how do post-translational modifications influence this?