ArticleExperimental cell research2011
A novel interaction of CLN3 with nonmuscle myosin-IIB and defects in cell motility of Cln3(-/-) cells.
Article in Experimental cell research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
30 citing papers in PubMed, 46 citations in OpenAlex.
- Toward Early Diagnosis and Therapeutic Discovery in CLN3 Disease: A Computational Biomarker Discovery Framework.medRxiv : the preprint server for health sciences · 2026Article
- Loss of CLN3 in microglia leads to impaired lipid metabolism and myelin turnover.Communications biology · 2024Article
- Lysosomal alterations and decreased electrophysiological activity in CLN3 disease patient-derived cortical neurons.Disease models & mechanisms · 2022Article
- CLN3, at the crossroads of endocytic trafficking.Neuroscience letters · 2021Article
- Review
- A human model of Batten disease shows role of CLN3 in phagocytosis at the photoreceptor-RPE interface.Communications biology · 2021Article
- Human INCL fibroblasts display abnormal mitochondrial and lysosomal networks and heightened susceptibility to ROS-induced cell death.PloS one · 2021Article
- Current Insights in Elucidation of Possible Molecular Mechanisms of the Juvenile Form of Batten Disease.International journal of molecular sciences · 2020Review
- Cellular models of Batten disease.Biochimica et biophysica acta. Molecular basis of disease · 2020Review
- The CLN3 gene and protein: What we know.Molecular genetics & genomic medicine · 2019Review
- Article
- Gene Therapy Corrects Brain and Behavioral Pathologies in CLN6-Batten Disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
- Multiple myosin motors interact with sodium/potassium-ATPase alpha 1 subunits.Molecular brain · 2018Article
- Lack of specificity of antibodies raised against CLN3, the lysosomal/endosomal transmembrane protein mutated in juvenile Batten disease.Bioscience reports · 2017Article
- Glial cells are functionally impaired in juvenile neuronal ceroid lipofuscinosis and detrimental to neurons.Acta neuropathologica communications · 2017Article
- Aberrant adhesion impacts early development in a Dictyostelium model for juvenile neuronal ceroid lipofuscinosis.Cell adhesion & migration · 2017Article
- Antigen presenting cell abnormalities in the Cln3(-/-) mouse model of juvenile neuronal ceroid lipofuscinosis.Biochimica et biophysica acta · 2016Article
- Human iPSC models of neuronal ceroid lipofuscinosis capture distinct effects of TPP1 and CLN3 mutations on the endocytic pathway.Human molecular genetics · 2014Article
- Article
- Life without double-headed non-muscle myosin II motor proteins.Frontiers in chemistry · 2014Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Juvenile neuronal ceroid lipofuscinosis (JNCL) is a pediatric lysosomal storage disorder characterized by accumulation of autofluorescent storage material and neurodegeneration, which result from mutations in CLN3. The function of CLN3, a lysosomal membrane protein, is currently unknown. We report that CLN3 interacts with cytoskeleton-associated nonmuscle myosin-IIB. Both CLN3 and myosin-IIB are ubiquitously expressed, yet mutations in either produce dramatic consequences in the CNS such as neurodegeneration in JNCL patients and Cln3(-/-) mouse models, or developmental deficiencies in Myh10(-/-) mice, respectively. A scratch assay revealed a migration defect associated with Cln3(-/-) cells. Inhibition of nonmuscle myosin-II with blebbistatin in WT cells resulted in a phenotype that mimics the Cln3(-/-) migration defect. Moreover, inhibiting lysosome function by treating cells with chloroquine exacerbated the migration defect in Cln3(-/-). Cln3(-/-) cells traversing a transwell filter under gradient trophic factor conditions displayed altered migration, further linking lysosomal function and cell migration. The myosin-IIB distribution in Cln3(-/-) cells is elongated, indicating a cytoskeleton defect caused by the loss of CLN3. In summary, cells lacking CLN3 have defects that suggest altered myosin-IIB activity, supporting a functional and physical interaction between CLN3 and myosin-IIB. We propose that the migration defect in Cln3(-/-) results, in part, from the loss of the CLN3-myosin-IIB interaction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.