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Article

HuD impairs neuromuscular junctions and induces apoptosis in human iPSC and Drosophila ALS models.

Nature communications - 7 Nov 2024

Silvestri Beatrice, Mochi Michela, Mawrie Darilang, de Turris Valeria, Colantoni Alessio, Borhy Beatrice, Medici Margherita, Anderson Eric Nathaniel, Garone Maria Giovanna, Zammerilla Christopher Patrick, Simula Marco, Ballarino Monica, Pandey Udai Bhan, Rosa Alessandro

Abstract excerpt

Defects at the neuromuscular junction (NMJ) are among the earliest hallmarks of amyotrophic lateral sclerosis (ALS). According to the "dying-back" hypothesis, NMJ disruption not only precedes but also triggers the subsequent degeneration of motoneurons in both sporadic (sALS) and familial (fALS) ALS. Using human induced pluripotent stem cells (iPSCs), we show that the RNA-binding protein HuD (ELAVL4) contributes...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 39511225
DOI: 10.1038/s41467-024-54004-8
PMCID: PMC11544248

Genes

FUS
ELAVL4

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

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HuD impairs neuromuscular junctions and induces apoptosis in human iPSC and Drosophila ALS models.PMID 39511225Read ↗

HuD (ELAVL4) gain-of-function impairs neuromuscular junctions and induces apoptosis in <i>in vitro</i> and <i>in vivo</i> models of amyotrophic lateral sclerosisSemantic proximity Read ↗

HuD (ELAVL4) gain-of-function impairs neuromuscular junctions and induces apoptosis in familial and sporadic amyotrophic lateral sclerosis modelsSemantic proximity Read ↗

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