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Article

A role for mitochondria-ER crosstalk in amyotrophic lateral sclerosis 8 pathogenesis.

Life science alliance - 1 Apr 2025

Wilson Cathal, Giaquinto Laura, Santoro Michele, Di Tullio Giuseppe, Morra Valentina, Kukulski Wanda, Venditti Rossella, Navone Francesca, Borgese Nica, De Matteis Maria Antonietta

Abstract excerpt

Protein aggregates in motoneurons, a pathological hallmark of amyotrophic lateral sclerosis, have been suggested to play a key pathogenetic role. ALS8, characterized by ER-associated inclusions, is caused by a heterozygous mutation in VAPB, which acts at multiple membrane contact sites between the ER and almost all other organelles. The link between protein aggregation and cellular dysfunction is unclear. A yeast...

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Topics

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Share to Amyotrophic Lateral Sclerosis
Share to Endoplasmic Reticulum

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Protein Aggregation, Pathological

Share to Saccharomyces cerevisiae

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Source

Open in PubMed Open full text

Identifiers

PMID: 39870504
DOI: 10.26508/lsa.202402907
PMCID: PMC11772500

Genes

VAPB

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

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A role for mitochondria-ER crosstalk in amyotrophic lateral sclerosis 8 pathogenesis.PMID 39870504Read ↗

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