ArticleJournal of cell science2015
CALHM1 ion channel elicits amyloid-β clearance by insulin-degrading enzyme in cell lines and in vivo in the mouse brain.
Article in Journal of cell science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Biology, function and structure of the calcium homeostasis modulator family.The Journal of physiology · 2025Review
- Ginsenoside Rg1 promotes β‑amyloid peptide degradation through inhibition of the ERK/PPARγ phosphorylation pathway in an Alzheimer's disease neuronal model.Experimental and therapeutic medicine · 2024Article
- Human CALHM5: Insight in large pore lipid gating ATP channel and associated neurological pathologies.Molecular and cellular biochemistry · 2021Review
- Resveratrol, Metabolic Dysregulation, and Alzheimer's Disease: Considerations for Neurogenerative Disease.International journal of molecular sciences · 2021Review
- Ginsenoside Rg1 reduces β‑amyloid levels by inhibiting CDΚ5‑induced PPARγ phosphorylation in a neuron model of Alzheimer's disease.Molecular medicine reports · 2020Article
- Structure and assembly of calcium homeostasis modulator proteins.Nature structural & molecular biology · 2020Article
- Article
- Validation of a priori candidate Alzheimer's disease SNPs with brain amyloid-beta deposition.Scientific reports · 2019Article
- Pioglitazone Reduces β Amyloid LevelsFrontiers in aging neuroscience · 2019Article
- The core sequence of PIF competes for insulin/amyloid β in insulin degrading enzyme: potential treatment for Alzheimer's disease.Oncotarget · 2018Article
- Blockade and knock-out of CALHM1 channels attenuate ischemic brain damage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Article
- CALHM3 Is Essential for Rapid Ion Channel-Mediated Purinergic Neurotransmission of GPCR-Mediated Tastes.Neuron · 2018Article
- Innate immune activation in Alzheimer's disease.Annals of translational medicine · 2018Review
- Insulin-degrading enzyme is not secreted from cultured cells.Scientific reports · 2018Article
- The NHAmerican journal of physiology. Cell physiology · 2017Article
- Ex vivoMolecular neurodegeneration · 2017Article
- A modification-specific peptide-based immunization approach using CRM197 carrier protein:Molecular medicine (Cambridge, Mass.) · 2017Article
- Neuroimaging Feature Terminology: A Controlled Terminology for the Annotation of Brain Imaging Features.Journal of Alzheimer's disease : JAD · 2017Article
- A mouse model of hereditary hemorrhagic telangiectasia generated by transmammary-delivered immunoblocking of BMP9 and BMP10.Scientific reports · 2016Article
- CALHM1 deficiency impairs cerebral neuron activity and memory flexibility in mice.Scientific reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease is characterized by amyloid-β (Aβ) peptide accumulation in the brain. CALHM1, a cell-surface Ca(2+) channel expressed in brain neurons, has anti-amyloidogenic properties in cell cultures. Here, we show that CALHM1 controls Aβ levels in vivo in the mouse brain through a previously unrecognized mechanism of regulation of Aβ clearance. Using pharmacological and genetic approaches in cell lines, we found that CALHM1 ion permeability and extracellular Ca(2+) were required for the Aβ-lowering effect of CALHM1. Aβ level reduction by CALHM1 could be explained by an increase in extracellular Aβ degradation by insulin-degrading enzyme (IDE), extracellular secretion of which was strongly potentiated by CALHM1 activation. Importantly, Calhm1 knockout in mice reduced IDE enzymatic activity in the brain, and increased endogenous Aβ concentrations by up to ∼50% in both the whole brain and primary neurons. Thus, CALHM1 controls Aβ levels in cell lines and in vivo by facilitating neuronal and Ca(2+)-dependent degradation of extracellular Aβ by IDE. This work identifies CALHM1 ion channel as a potential target for promoting amyloid clearance in Alzheimer's disease.
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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.