Disruption of ER‐mitochondria tethering and signalling in C9orf72‐associated amyotrophic lateral scl...
Disruption of ER‐mitochondria tethering and signalling in C9orf72‐associated amyotrophic lateral sclerosis and frontotemporal dementia
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Author / Creator
Gomez‐Suaga, Patricia , Mórotz, Gábor M. , Markovinovic, Andrea , Martín‐Guerrero, Sandra M. , Preza, Elisavet , Arias, Natalia , Mayl, Keith , Aabdien, Afra , Gesheva, Vesela , Nishimura, Agnes , Annibali, Ambra , Lee, Younbok , Mitchell, Jacqueline C. , Wray, Selina , Shaw, Christopher , Noble, Wendy and Miller, Christopher C. J.
Publisher
England: John Wiley & Sons, Inc
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Language
English
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Publisher
England: John Wiley & Sons, Inc
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Contents
Hexanucleotide repeat expansions in C9orf72 are the most common cause of familial amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). The mechanisms by which the expansions cause disease are not properly understood but a favoured route involves its translation into dipeptide repeat (DPR) polypeptides, some of which are neurotoxic...
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Full title
Disruption of ER‐mitochondria tethering and signalling in C9orf72‐associated amyotrophic lateral sclerosis and frontotemporal dementia
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TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8844122
Permalink
https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8844122
Other Identifiers
ISSN
1474-9718
E-ISSN
1474-9726
DOI
10.1111/acel.13549