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Hong-Yu Hu

Laboratory of Molecular Biology
Chinese Academy of Sciences

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O-GlcNAcylation of TDP-43 suppresses proteinopathies and promotes TDP-43's mRNA splicing activity.

2021 EMBO Reports
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PolyQ-expanded proteins impair cellular proteostasis of ataxin-3 through sequestering the co-chaperone HSJ1 into aggregates.

2021 Scientific Reports
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Solid-state NMR reveals the structural transformation of the TDP-43 amyloidogenic region upon fibrillation

2020 Journal of the American Chemical Society
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Modified subintimal plaque modification improving future recanalization of chronic total occlusion percutaneous coronary intervention

2020 Journal of Geriatric Cardiology
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Author Correction: Structural and dynamic studies reveal that the Ala-rich region of ataxin-7 initiates α-helix formation of the polyQ tract but suppresses its aggregation.

2020 Scientific Reports
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Structural and dynamic studies reveal that the Ala-rich region of ataxin-7 initiates α-helix formation of the polyQ tract but suppresses its aggregation

2019 Scientific Reports
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HSP90 recognizes the N-terminus of huntingtin involved in regulation of huntingtin aggregation by USP19

2017 Scientific Reports
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The N-terminal dimerization is required for TDP-43 splicing activity

2017 Scientific Reports
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Two mutations G335D and Q343R within the amyloidogenic core region of TDP-43 influence its aggregation and inclusion formation

2016 Scientific Reports
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Cytoplasmic Ubiquitin-Specific Protease 19 (USP19) Modulates Aggregation of Polyglutamine-Expanded Ataxin-3 and Huntingtin through the HSP90 Chaperone

2016 PLOS ONE
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