Evaluates how phosphorylation affects the compactness of the tau protein in neurodegenerative diseases, suggesting implications for Alzheimer's research.
The proline-rich region of the tubulin-associated unit (TAU) protein is of substantial interest in understanding neurodegenerative diseases due to its interaction with bridging integrator 1 (BIN1). The associated gene BIN1 is substantially associated with the development of Alzheimer's disease. Previous studies have underlined the importance of the conformation of the proline-rich region of TAU and the effect of its phosphorylation. In this study, we investigate the change in compactness between a four times phosphorylated TAU fragment (210-240) compared to the unphosphorylated (non-P) form using computational means. We apply our Ensemble Reconstruction from Fragments (ERF) approach to create two unbiased conformational ensembles from which a reweighted ensemble is derived that agrees with observables from nuclear magnetic resonance experiments. The resulting shift of the radius of gyration indicates a preference for relatively compact conformations for the non-P form, while the restraints derived from the experimental data do not substantially influence the compactness of the phosphorylated peptide.
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Stöckelmaier et al. (2026) studied this question.
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