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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 scl...

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8844122

Disruption of ER‐mitochondria tethering and signalling in C9orf72‐associated amyotrophic lateral sclerosis and frontotemporal dementia

About this item

Full title

Disruption of ER‐mitochondria tethering and signalling in C9orf72‐associated amyotrophic lateral sclerosis and frontotemporal dementia

Publisher

England: John Wiley & Sons, Inc

Journal title

Aging cell, 2022-02, Vol.21 (2), p.e13549-n/a

Language

English

Formats

Publication information

Publisher

England: John Wiley & Sons, Inc

More information

Scope and Contents

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...

Alternative Titles

Full title

Disruption of ER‐mitochondria tethering and signalling in C9orf72‐associated amyotrophic lateral sclerosis and frontotemporal dementia

Identifiers

Primary Identifiers

Record Identifier

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

How to access this item