Loss of TDP-43 promotes somatic CAG repeat expansion in Huntington’s disease knock-in mice
Author:
Publisher
Elsevier BV
Subject
General Neuroscience
Reference46 articles.
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3. Lack of association of somatic CAG repeat expansion with striatal neurodegeneration in HD knock-in animal models;Bai;Hum. Mol. Genet.,2021
4. Nuclear factor TDP-43 and SR proteins promote in vitro and in vivo CFTR exon 9 skipping;Buratti;EMBO J.,2001
5. The N-terminus of TDP-43 promotes its oligomerization and enhances DNA binding affinity;Chang;Biochem Biophys. Res. Commun.,2012
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1. The role of N6-methyladenosine modification in neurodegenerative diseases;Ageing and Neurodegenerative Diseases;2024-09-05
2. TDP43 and huntingtin Exon-1 undergo a conformationally specific interaction that strongly alters the fibril formation of both proteins;Journal of Biological Chemistry;2024-09
3. HAP40 modulates mutant Huntingtin aggregation and toxicity in Huntington’s disease mice;Cell Death & Disease;2024-05-14
4. Huntington’s Disease: Complex Pathogenesis and Therapeutic Strategies;International Journal of Molecular Sciences;2024-03-29
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