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Article

Caenorhabditis elegans homologues of the CLN3 gene, mutated in juvenile neuronal ceroid lipofuscinosis.

European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society - 1 Jan 2001

De Voer G, Jansen G, van Ommen G J, Peters D J, Taschner P E

Abstract excerpt

Neuronal ceroid lipofuscinoses (NCLs) are the most common hereditary neurodegenerative disorders of childhood. The first symptom of this heterogeneous group of devastating lysosomal storage diseases is progressive visual failure. The different forms of NCL can be distinguished by age of onset, clinical features and the characteristics of the accumulated materials. The juvenile form, Batten-Spielmeyer-Vogt disease...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 11588981
DOI: 10.1053/ejpn.2000.0446

Genes

CLN3
NCL

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.

Related research

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Caenorhabditis elegans homologues of the CLN3 gene, mutated in juvenile neuronal ceroid lipofuscinosis.PMID 11588981Read ↗

Deletion of the Caenorhabditis elegans homologues of the CLN3 gene, involved in human juvenile neuronal ceroid lipofuscinosis, causes a mild progeric phenotype.Semantic proximity Read ↗

A function retained by the common mutant CLN3 protein is responsible for the late onset of juvenile neuronal ceroid lipofuscinosis.Semantic proximity Read ↗

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Autophagic vacuolar myopathy is a common feature of CLN 3 diseaseSemantic proximity Read ↗

CLC-3 deficiency leads to phenotypes similar to human neuronal ceroid lipofuscinosis.Semantic proximity Read ↗

CLN3 deficiency leads to neurological and metabolic perturbations during early developmentSemantic proximity Read ↗

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