Sup35 is a prion-like protein from yeast and shares the ability to transmit its aberrant fold and to aggregate into amyloid fibrils. 7GNNQQNY13 from the prion-determining domain of Sup35 was reported to form an amyloid. We first investigated the self-aggregation transition behavior of GNNQQNY to the β-sheet amyloid state under various conditions. Mechanical stirring using a magnetic bar resulted in accelerated aggregation of the GNNQQNY. The aggregation rate of GNNQQNY was also dependent on its concentration; the higher the GNNQQNY concentration, the faster the aggregation. Circular dichroism and Fourier transform-infrared spectral data indicated the formation of the β-sheet structure in the GNNQQNY aggregates. The fluorescence experiments using an amyloid-specific thioflavin T also demonstrated that the GNNQQNY aggregates formed the amyloid structures. The amyloid structure of the GNNQQNY aggregates served as seeds for the elongation of the monomeric GNNQQNY in the solution state. We further studied the ability of the GNNQQNY amyloid fibrils to act as seeds for the elongation of the amyloid-forming monomeric proteins (albumin, lysozyme and insulin). The cross-seeding experiments suggested that the GNNQQNY aggregate could possibly promote the amyloid fibril formation of heterogeneous insulin. The inverse monomeric GNNQQNY would have a binding capacity for the heterogeneous already-formed amyloid-β fibrils on a mice brain section. These basic data could be informative for elucidating the pathogenic and/or propagation mechanisms of prion agents and developing effective therapeutics and/or diagnosis for prion diseases.
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Evidence ID | Analyze ID | Gene/Complex | Systematic Name/Complex Accession | Qualifier | Gene Ontology Term ID | Gene Ontology Term | Aspect | Annotation Extension | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Phenotype | Experiment Type | Experiment Type Category | Mutant Information | Strain Background | Chemical | Details | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Disease Ontology Term | Disease Ontology Term ID | Qualifier | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Regulator | Regulator Systematic Name | Target | Target Systematic Name | Direction | Regulation of | Happens During | Regulator Type | Direction | Regulation Of | Happens During | Method | Evidence | Strain Background | Reference |
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Site | Modification | Modifier | Source | Reference |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Allele | Assay | Annotation | Action | Phenotype | SGA score | P-value | Source | Reference | Note |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Assay | Annotation | Action | Modification | Source | Reference | Note |
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Complement ID | Locus ID | Gene | Species | Gene ID | Strain background | Direction | Details | Source | Reference |
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Evidence ID | Analyze ID | Dataset | Description | Keywords | Number of Conditions | Reference |
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Evidence ID | Analyze ID | File | Description |
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