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Article

ERp57 is protective against mutant SOD1-induced cellular pathology in amyotrophic lateral sclerosis.

Human molecular genetics - 15 Apr 2018

Parakh Sonam, Jagaraj Cyril J, Vidal Marta, Ragagnin Audrey M G, Perri Emma R, Konopka Anna, Toth Reka P, Galper Jasmin, Blair Ian P, Thomas Colleen J, Walker Adam K, Yang Shu, Spencer Damian M, Atkin Julie D

Abstract excerpt

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder and mutations in superoxide dismutase 1 (SOD1) account for 20% of familial ALS cases. The aetiology of ALS remains unclear, but protein misfolding, endoplasmic reticulum (ER) stress and neuronal apoptosis are implicated. We previously established that protein disulphide isomerase (PDIA1) is protective against ER stress and apoptosis in...

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Share to Amyotrophic Lateral Sclerosis
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 29409023
DOI: 10.1093/hmg/ddy041

Genes

SOD1
PDIA3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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ERp57 is protective against mutant SOD1-induced cellular pathology in amyotrophic lateral sclerosis.PMID 29409023Read ↗

Protein Disulfide Isomerase Endoplasmic Reticulum Protein 57 (ERp57) is Protective Against ALS-Associated Mutant TDP-43 in Neuronal Cells.Semantic proximity Read ↗

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