Cross-seeding by prion protein inactivates TDP-43.

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作者： Stella A,Polido ^[1] ; Cristiana,Stuani ^[2] ; Aaron,Voigt ^[3] ; Papiya,Banik ^[1] ; Janine,Kamps ^[1] ; Verian,Bader ^[4] ; Prerna,Grover ^[1] ; Laura J,Krause ^[5] ; Inga,Zerr ^[1] ; Jakob,Matschke ^[4] ; Markus,Glatzel ^[5] ; Konstanze F,Winklhofer ^[6] ; Emanuele,Buratti ^[7] ; Jörg,Tatzelt ^[7]

作者单位： Department of Biochemistry of Neurodegenerative Diseases, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, 44801 Bochum, Germany. ^[1] International Centre for Genetic Engineering and Biotechnology (ICGEB), 34149 Trieste, Italy. ^[2] Department of Neurology, Medical Faculty, University Hospital, RWTH Aachen University, 52074 Aachen, Germany. ^[3] Cluster of Excellence RESOLV, Ruhr University Bochum, 44801 Bochum, Germany. ^[4] Department of Molecular Cell Biology, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, 44801 Bochum, Germany. ^[5] Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany. ^[6] Institute of Neuropathology, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany. ^[7]

关键词 ER import RNA splicing TDP-43 neurodegeneration prion protein aggregation

主题词动物(Animals);人类(Humans);克-亚综合征(Creutzfeldt-Jakob Syndrome);DNA结合蛋白质类(DNA-Binding Proteins);哺乳动物(Mammals);朊病毒病(Prion Diseases);朊病毒(Prions)

DOI 10.1093/brain/awad289

PMID 37669322

发布时间 2024-03-06

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