ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
CLHM-1 is a functionally conserved and conditionally toxic Ca2+-permeable ion channel in Caenorhabditis elegans.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 41 citations in OpenAlex.
- Article
- Superoxide dismutase impacts extracellular vesicle shedding and uptake.Free radical biology & medicine · 2026Article
- Phosphatidylinositol 4,5-bisphosphate impacts extracellular vesicle shedding from C. elegans ciliated sensory neurons.Journal of cell science · 2025Article
- Identification and classification of ion-channels across the tree of life provide functional insights into understudied CALHM channels.bioRxiv : the preprint server for biology · 2025Article
- Article
- Phosphatidylinositol 4,5-bisphosphate Impacts Extracellular Vesicle Shedding frombioRxiv : the preprint server for biology · 2025Article
- Biology, function and structure of the calcium homeostasis modulator family.The Journal of physiology · 2025Review
- A higher dysregulation burden of brain DNA methylation in female patients implicated in the sex bias of Schizophrenia.Molecular psychiatry · 2023Article
- A Higher Dysregulation Burden of Brain DNA Methylation in Female Patients Implicated in the Sex Bias of Schizophrenia.Research square · 2023Article
- Kinesin-2 motors differentially impact biogenesis of extracellular vesicle subpopulations shed from sensory cilia.iScience · 2022Article
- Noncanonical necrosis in 2 different cell types in a Caenorhabditis elegans NAD+ salvage pathway mutant.G3 (Bethesda, Md.) · 2022Article
- Modeling Alzheimer's Disease inBiomedicines · 2022Review
- Suppression of Selective Voltage-Gated Calcium Channels Alleviates Neuronal Degeneration and Dysfunction through Glutathione S-Transferase-Mediated Oxidative Stress Resistance in aOxidative medicine and cellular longevity · 2022Article
- Human CALHM5: Insight in large pore lipid gating ATP channel and associated neurological pathologies.Molecular and cellular biochemistry · 2021Review
- On the molecular nature of large-pore channels.Journal of molecular biology · 2021Review
- Elevating the Levels of Calcium Ions Exacerbate Alzheimer's Disease via Inducing the Production and Aggregation of β-Amyloid Protein and Phosphorylated Tau.International journal of molecular sciences · 2021Review
- Taste transduction and channel synapses in taste buds.Pflugers Archiv : European journal of physiology · 2021Review
- Cryo-electron microscopy structure of CLHM1 ion channel from Caenorhabditis elegans.Protein science : a publication of the Protein Society · 2020Article
- Cryo-EM structures of calcium homeostasis modulator channels in diverse oligomeric assemblies.Science advances · 2020Article
- Structures of CALHM channels revealed.Nature structural & molecular biology · 2020Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Disruption of neuronal Ca(2+) homeostasis contributes to neurodegenerative diseases through mechanisms that are not fully understood. A polymorphism in CALHM1, a recently described ion channel that regulates intracellular Ca(2+) levels, is a possible risk factor for late-onset Alzheimer's disease. Since there are six potentially redundant CALHM family members in humans, the physiological and pathophysiological consequences of CALHM1 function in vivo remain unclear. The nematode Caenorhabditis elegans expresses a single CALHM1 homolog, CLHM-1. Here we find that CLHM-1 is expressed at the plasma membrane of sensory neurons and muscles. Like human CALHM1, C. elegans CLHM-1 is a Ca(2+)-permeable ion channel regulated by voltage and extracellular Ca(2+). Loss of clhm-1 in the body-wall muscles disrupts locomotory kinematics and biomechanics, demonstrating that CLHM-1 has a physiologically significant role in vivo. The motility defects observed in clhm-1 mutant animals can be rescued by muscle-specific expression of either C. elegans CLHM-1 or human CALHM1, suggesting that the function of these proteins is conserved in vivo. Overexpression of either C. elegans CLHM-1 or human CALHM1 in neurons is toxic, causing degeneration through a necrotic-like mechanism that is partially Ca(2+) dependent. Our data show that CLHM-1 is a functionally conserved ion channel that plays an important but potentially toxic role in excitable cell function.
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