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Current Protein & Peptide Science|July 12, 2016
Study of Protein Amyloid-Like Aggregates by Solid-State Circular Dichroism SpectroscopyHong-Yu Hu, Lei-Lei Jiang, Jun-Ye HongScientific Reports|April 10, 2021
PolyQ-expanded proteins impair cellular proteostasis of ataxin-3 through sequestering the co-chaperone HSJ1 into aggregatesHong-Wei Yue, Jun-Ye Hong, Shu-Xian Zhang, et al.FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology|February 7, 2018
PolyQ-expanded huntingtin and ataxin-3 sequester ubiquitin adaptors hHR23B and UBQLN2 into aggregates via conjugated ubiquitinHui Yang, Hong-Wei Yue, Wen-Tian He, et al.The Biochemical Journal|October 23, 2020
Domain interactions reveal auto-inhibition of the deubiquitinating enzyme USP19 and its activation by HSP90 in the modulation of huntingtin aggregationWei Xue, Shu-Xian Zhang, Wen-Tian He, et al.Scientific Reports|November 3, 2017
HSP90 recognizes the N-terminus of huntingtin involved in regulation of huntingtin aggregation by USP19Wen-Tian He, Wei Xue, Yong-Guang Gao, et al.Acta Biochimica Et Biophysica Sinica|May 12, 2023
Coaggregation of polyglutamine (polyQ) proteins is mediated by polyQ-tract interactions and impairs cellular proteostasisJun-Ye Hong, Jian-Yang Wang, Hong-Wei Yue, et al.Scientific Reports|May 18, 2019
Structural and dynamic studies reveal that the Ala-rich region of ataxin-7 initiates α-helix formation of the polyQ tract but suppresses its aggregationJun-Ye Hong, Dong-Dong Wang, Wei Xue, et al.Scientific Reports|June 11, 2020
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 aggregationJun-Ye Hong, Wei Xue, Hong-Wei Yue, et al.Scientific Reports|July 23, 2017
The N-terminal dimerization is required for TDP-43 splicing activityLei-Lei Jiang, Wei Xue, Jun-Ye Hong, et al.Pageof 1