The node-based overlap between this network and other networks is calculated as the Szymkiewicz-Simpson coefficient of their respective nodes. Up to the top 10 are shown below.
|Tau Modifications v1.9.5
|Tau oligomers and tau toxicity in neurodegenerative disease v1.0.0
|Extracellular low-n oligomers of tau cause selective synaptotoxicity without affecting cell viability v1.0.0
|Caenorhabditis elegans models of tauopathy v1.0.0
|Inert and seed-competent tau monomers suggest structural origins of aggregation v1.0.0
|Pathological missorting of endogenous MAPT/Tau in neurons caused by failure of protein degradation systems v1.0.1
|Molecular chaperones and regulation of tau quality control: strategies for drug discovery in tauopathies v1.0.0
|Tau Protein Hyperphosphorylation and Aggregation in Alzheimer’s Disease and Other Tauopathies, and Possible Neuroprotective Strategies v1.0.0
|TAU and Interaction Partners v1.2.5
|PP2A and Alzheimer Disease v1.0.0
Our finding that the resulting Tau species with phosphorylation at Ser202/Th205, but with a disrupted turn-like structure, forms abundant fibers detectable by thioflavin fluorescence or electron microscopy (Figs. 2 and 4) suggests the initial turn-like structure induced by the phosphorylation of only Ser202 and Thr205 is protective against aggregation.
Indeed, Tau phosphorylation at the three positions, Ser202/Thr205/Ser208, while not at Ser262, is sufficient to induce aggregation without the addition of any exogenous aggregation inducer.
Phosphorylation at Ser208 might be catalyzed by Casein kinase 1 (44), and its identification as a potential site for O-GlcNacylation (45) points to the important role of this residue.
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.