ArticleAging cell2015
CALHM1 and its polymorphism P86L differentially control Ca²⁺homeostasis, mitogen-activated protein kinase signaling, and cell vulnerability upon exposure to amyloid β.
Article in Aging cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Role of Mitochondrial Calcium Dysregulation in Alzheimer's Disease Pathogenesis.Molecular neurobiology · 2025Review
- Volatile oil ofFrontiers in pharmacology · 2025Review
- L-Glutamate Regulates Npy via the mGluR4-CaInternational journal of molecular sciences · 2024Article
- Unnexin is a protein subunit of a large-pore channel expressed by unicellular organisms.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Microglial Calhm2 regulates neuroinflammation and contributes to Alzheimer's disease pathology.Science advances · 2021Article
- Interrelation between ROS and CaRedox biology · 2020Review
- Cryo-electron microscopy structure of CLHM1 ion channel from Caenorhabditis elegans.Protein science : a publication of the Protein Society · 2020Article
- The mJournal of experimental & clinical cancer research : CR · 2019Article
- Calhm2 governs astrocytic ATP releasing in the development of depression-like behaviors.Molecular psychiatry · 2018Article
- Autophagy Activation Alleviates Amyloid-β-Induced Oxidative Stress, Apoptosis and Neurotoxicity in Human Neuroblastoma SH-SY5Y Cells.Neurotoxicity research · 2017Article
- Sorcin Predicts Poor Prognosis and Promotes Metastasis by Facilitating Epithelial-mesenchymal Transition in Hepatocellular Carcinoma.Scientific reports · 2017Article
- Calcium homeostasis modulator (CALHM) ion channels.Pflugers Archiv : European journal of physiology · 2016Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mutated form of the Ca²⁺channel CALHM1 (Ca²⁺homeostasis modulator 1), P86L-CALHM1, has been correlated with early onset of Alzheimer's disease (AD). P86L-CALHM1 increases production of amyloid beta (Aβ) upon extracellular Ca²⁺removal and its subsequent addback. The aim of this study was to investigate the effect of the overexpression of CALHM1 and P86L-CALHM, upon Aβ treatment, on the following: (i) the intracellular Ca²⁺signal pathway; (ii) cell survival proteins ERK1/2 and Ca²⁺/cAMP response element binding (CREB); and (iii) cell vulnerability after treatment with Aβ. Using aequorins to measure the effect of nuclear Ca²⁺concentrations ([Ca²⁺]n ) and cytosolic Ca²⁺concentrations ([Ca²⁺]c ) on Ca²⁺entry conditions, we observed that baseline [Ca²⁺]n was higher in CALHM1 and P86L-CALHM1 cells than in control cells. Moreover, exposure to Aβ affected [Ca²⁺]c levels in HeLa cells overexpressing CALHM1 and P86L-CALHM1 compared with control cells. Treatment with Aβ elicited a significant decrease in the cell survival proteins p-ERK and p-CREB, an increase in the activity of caspases 3 and 7, and more frequent cell death by inducing early apoptosis in P86L-CALHM1-overexpressing cells than in CALHM1 or control cells. These results suggest that in the presence of Aβ, P86L-CALHM1 shifts the balance between neurodegeneration and neuronal survival toward the stimulation of pro-cytotoxic pathways, thus potentially contributing to its deleterious effects in AD.
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