ArticleScientific reports2016
Clec16a is Critical for Autolysosome Function and Purkinje Cell Survival.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- Is DEXI a Multiple Sclerosis Susceptibility Gene?International journal of molecular sciences · 2025Review
- Autophagy and proteasomes in thymic epithelial cells: essential bulk protein degradation systems for immune homeostasis maintenance.Frontiers in immunology · 2024Review
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- CLEC16A interacts with retromer and TRIM27, and its loss impairs endosomal trafficking and neurodevelopment.Human genetics · 2023Article
- Article
- Review
- Autoimmune Disease AssociatedFrontiers in genetics · 2022Article
- Inducible knockout of Clec16a in mice results in sensory neurodegeneration.Scientific reports · 2021Article
- JAK/STAT inhibitor therapy partially rescues the lipodystrophic autoimmune phenotype in Clec16a KO mice.Scientific reports · 2021Article
- Mitophagy protects β cells from inflammatory damage in diabetes.JCI insight · 2020Article
- Genome-Wide Scan for Five Brain Oscillatory Phenotypes Identifies a New QTL Associated with Theta EEG Band.Brain sciences · 2020Article
- CYLD exaggerates pressure overload-induced cardiomyopathy via suppressing autolysosome efflux in cardiomyocytes.Journal of molecular and cellular cardiology · 2020Article
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- 9q34 & 16p13 chromosome duplications in autism.AME case reports · 2020Article
- Post-mortem multiple sclerosis lesion pathology is influenced by single nucleotide polymorphisms.Brain pathology (Zurich, Switzerland) · 2020Article
- Golgi Apparatus: A Potential Therapeutic Target for Autophagy-Associated Neurological Diseases.Frontiers in cell and developmental biology · 2020Review
- The proteasome regulator PI31 is required for protein homeostasis, synapse maintenance, and neuronal survival in mice.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- The Genetic Contribution to Type 1 Diabetes.Current diabetes reports · 2019Review
- In vivo identification of GTPase interactors by mitochondrial relocalization and proximity biotinylation.eLife · 2019Article
- Review
Corrections and comments
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Authors and funding
23 authors at 5 institutions in 2 countries.
Funding
Abstract
CLEC16A is in a locus genetically linked to autoimmune diseases including multiple sclerosis, but the function of this gene in the nervous system is unknown. Here we show that two mouse strains carrying independent Clec16a mutations developed neurodegenerative disease characterized by motor impairments and loss of Purkinje cells. Neurons from Clec16a-mutant mice exhibited increased expression of the autophagy substrate p62, accumulation of abnormal intra-axonal membranous structures bearing the autophagy protein LC3, and abnormal Golgi morphology. Multiple aspects of endocytosis, lysosome and Golgi function were normal in Clec16a-deficient murine embryonic fibroblasts and HeLa cells. However, these cells displayed abnormal bulk autophagy despite unimpaired autophagosome formation. Cultured Clec16a-deficient cells exhibited a striking accumulation of LC3 and LAMP-1 positive autolysosomes containing undigested cytoplasmic contents. Therefore Clec16a, an autophagy protein that is critical for autolysosome function and clearance, is required for Purkinje cell survival.
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