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Article

Neuronal ceroid lipofuscinosis protein CLN3 interacts with motor proteins and modifies location of late endosomal compartments.

Cellular and molecular life sciences : CMLS - 1 Jun 2012

Uusi-Rauva Kristiina, Kyttälä Aija, van der Kant Rik, Vesa Jouni, Tanhuanpää Kimmo, Neefjes Jacques, Olkkonen Vesa M, Jalanko Anu

Abstract excerpt

CLN3 is an endosomal/lysosomal transmembrane protein mutated in classical juvenile onset neuronal ceroid lipofuscinosis, a fatal inherited neurodegenerative lysosomal storage disorder. The function of CLN3 in endosomal/lysosomal events has remained elusive due to poor understanding of its interactions in these compartments. It has previously been shown that the localisation of late endosomal/lysosomal...

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Share to Endosomes
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Membrane Glycoproteins

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Share to Molecular Motor Proteins

Share to Neuronal Ceroid-Lipofuscinoses

Share to rab GTP-Binding Proteins

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Source

Open in PubMed Open full text

Identifiers

PMID: 22261744
DOI: 10.1007/s00018-011-0913-1
PMCID: PMC11114557

Genes

CLN3
RILP

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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Neuronal ceroid lipofuscinosis protein CLN3 interacts with motor proteins and modifies location of late endosomal compartments.PMID 22261744Read ↗

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Defective intracellular transport of CLN3 is the molecular basis of Batten disease (JNCL)Semantic proximity Read ↗

The intracellular location and function of proteins of neuronal ceroid lipofuscinoses.Semantic proximity Read ↗

CLN3 regulates endosomal function by modulating Rab7A activitySemantic proximity Read ↗

Biosynthesis and Intracellular Targeting of the CLN3 Protein Defective in Batten DiseaseSemantic proximity Read ↗

Interconnections of CLN3, Hook1 and Rab proteins link Batten disease to defects in the endocytic pathwaySemantic proximity Read ↗

AP-1 and AP-3 facilitate lysosomal targeting of Batten disease protein CLN3 via its dileucine motif.Semantic proximity Read ↗

KCTD7 mutations impair the trafficking of lysosomal enzymes through CLN5 accumulation to cause neuronal ceroid lipofuscinoses.Semantic proximity Read ↗

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