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Nup62 is recruited to pathological condensates and promotes TDP-43 insolubility in C9orf72 and sporadic ALS/FTLD.

2021-02-19

Abstract excerpt

<title>Abstract</title> <p>Amyotrophic lateral sclerosis (ALS) and Frontotemporal Lobar Degeneration (FTLD) share clinical, neuropathological, and genetic features. This includes common genetic disease-causing mutations such as the expanded G4C2 repeat in the C9orf72 gene (C9-ALS/FTLD) and cytoplasmic and insoluble protein depositions of the TDP-43 in degenerating regions of the brain and spinal cord. Proposed me...

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Literature Corpus work
a2ee3937-e306-5585-95ce-e173652ea31e
DOI
10.21203/rs.3.rs-144654/v1
Open publication

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Nup62 is recruited to pathological condensates and promotes TDP-43 insolubility in C9orf72 and sporadic ALS/FTLD.DOI 10.21203/rs.3.rs-144654/v1
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